Pub Date : 2020-01-08DOI: 10.3760/CMA.J.ISSN.1001-9030.2020.01.023
Jun Hong, Jingquan Liu, Fangxiao Gong, Lingzhi Jiang, Shijing Mo, Minhua Chen, Xianghong Yang, R. Sun
Objective To investigate the effects of microRNA (miRNA, miR)-224 level changes on the lipopolysaccharide (LPS)-induced injury of pulmonary microvascular endothelium cells (PMVECs) and its mechanism. Methods Primary PMVECs were isolated from clean-level BALB/c mice and cultured in vitro. In order to induce cells injury, 1.0 mg/L LPS was used to treat PMVECs. MiR-224 inhibitor and p21 siRNA were transfected for silencing miR-224 and p21, respectively. The cell viability and apoptosis rate of PMVECs were detected by cell counting kit-8 reagent and flow cytometry, respectively. The changes of miR-224 and p21 were detected by fluorescent quantitative polymerase chain reaction (FQ-PCR) and Western blotting. Dual-luciferase reporter assay was used to determine the target relationship between miR-224 and p21. T-test was used to compare the mean between the two groups and the pairwise comparison of the mean among multiple groups was conducted by LSD test on the basis of one-way analysis of variance. Results After LPS treatment, the relative cell viability decreased to (42.333±7.586)% and apoptosis rate increased to (32.141±2.449)% as compared with non-LPS treated cells. Meanwhile, the level of miR-224 increased to 1.791±0.167 with a decreased p21 mRNA expression (0.527±0.058) (t=8.532, 7.261, 7.113 and 8.467, P<0.01). As compared with simple LPS treated cells, PMVECs transfected with miR-224 inhibitor showed lower cell inhibition and apoptosis rate after LPS treatment (F=62.618 and 32.643, P<0.01). However, p21 knock-down could antagonize the protective effect of miR-224. Conclusion MiR-224 may mediate the LPS-induced injury of PMVECs via targeting p21. MiR-224 could be a therapy target for acute lung injury/acute respiratory distress syndrome after sepsis. Key words: Sepsis; Lipopolysaccharide; Endotheliumcell; Acute lung injury; Acute respiratory distress syndrome; MicroRNA; P21
{"title":"MicroRNA-224 mediates lipopolysaccharide-induced injury of pulmonary microvascular endothelium cells via regulating p21","authors":"Jun Hong, Jingquan Liu, Fangxiao Gong, Lingzhi Jiang, Shijing Mo, Minhua Chen, Xianghong Yang, R. Sun","doi":"10.3760/CMA.J.ISSN.1001-9030.2020.01.023","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2020.01.023","url":null,"abstract":"Objective \u0000To investigate the effects of microRNA (miRNA, miR)-224 level changes on the lipopolysaccharide (LPS)-induced injury of pulmonary microvascular endothelium cells (PMVECs) and its mechanism. \u0000 \u0000 \u0000Methods \u0000Primary PMVECs were isolated from clean-level BALB/c mice and cultured in vitro. In order to induce cells injury, 1.0 mg/L LPS was used to treat PMVECs. MiR-224 inhibitor and p21 siRNA were transfected for silencing miR-224 and p21, respectively. The cell viability and apoptosis rate of PMVECs were detected by cell counting kit-8 reagent and flow cytometry, respectively. The changes of miR-224 and p21 were detected by fluorescent quantitative polymerase chain reaction (FQ-PCR) and Western blotting. Dual-luciferase reporter assay was used to determine the target relationship between miR-224 and p21. T-test was used to compare the mean between the two groups and the pairwise comparison of the mean among multiple groups was conducted by LSD test on the basis of one-way analysis of variance. \u0000 \u0000 \u0000Results \u0000After LPS treatment, the relative cell viability decreased to (42.333±7.586)% and apoptosis rate increased to (32.141±2.449)% as compared with non-LPS treated cells. Meanwhile, the level of miR-224 increased to 1.791±0.167 with a decreased p21 mRNA expression (0.527±0.058) (t=8.532, 7.261, 7.113 and 8.467, P<0.01). As compared with simple LPS treated cells, PMVECs transfected with miR-224 inhibitor showed lower cell inhibition and apoptosis rate after LPS treatment (F=62.618 and 32.643, P<0.01). However, p21 knock-down could antagonize the protective effect of miR-224. \u0000 \u0000 \u0000Conclusion \u0000MiR-224 may mediate the LPS-induced injury of PMVECs via targeting p21. MiR-224 could be a therapy target for acute lung injury/acute respiratory distress syndrome after sepsis. \u0000 \u0000 \u0000Key words: \u0000Sepsis; Lipopolysaccharide; Endotheliumcell; Acute lung injury; Acute respiratory distress syndrome; MicroRNA; P21","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"37 1","pages":"81-83"},"PeriodicalIF":0.0,"publicationDate":"2020-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41896948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective To establish a stable and reliable mouse atherosclerotic (AS) model, and standardize principal process of AS model identification. Methods The mouse AS model was developed by feeding apolipoprotein E (ApoE) gene knockout mice (ApoE-/-) on high-fat diet (hfd). Sixteen weeks later, the body weight, blood sugar, blood pressure and blood lipid were determined, and aortas were stained with oil red O and hematoxylin to evaluate the AS plaque. Results Cholesterol [(20.09±1.02) mmol/L] and low density lipoprotein cholesterol [(6.84±0.65) mmol/L] of ApoE-/- mice with hfd were significantly increased as compared with that in C57BL/6J normal diet (nd) group [total cholesterol (TC): (2.04±0.07) mmol/L, LDL-C: (0.25±0.01) mmol/L, F=190.543, 82.795, P<0.01]. Oil Red O staining of entire aorta showed that AS lesion size in ApoE-/-+ hfd mice [(22.09±3.49)%] was dramatically increased as compared with that in ApoE-/-+ nd mice [(1.46±0.96)%, F=118.558, P<0.01]. Similar result was obtained from cross-sections of aortic root analysis. Hematoxylin and eosin (HE) staining of cross-sections of aorta root showed typical As plaques. Conclusion The hfd treatment successfully promoted AS development in ApoE-/- mice. The process of gene identification-general situation analysis-blood lipid analysis-morphologic analysis was established to verify AS model. The establishment of mouse AS model provides a valuable tool for the study of AS-related diseases in vivo. Key words: Atherosclerosis; Gene knock out mice; Low density lipoprotein; Cholesterol; Lorta
{"title":"Establishment of mouse atherosclerotic model","authors":"Yiquan Dai, Xiaoxiao Yan, Xiao‐Ru Liu, Yichen Lin, Hongyu Chen","doi":"10.3760/CMA.J.ISSN.1001-9030.2020.01.050","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2020.01.050","url":null,"abstract":"Objective \u0000To establish a stable and reliable mouse atherosclerotic (AS) model, and standardize principal process of AS model identification. \u0000 \u0000 \u0000Methods \u0000The mouse AS model was developed by feeding apolipoprotein E (ApoE) gene knockout mice (ApoE-/-) on high-fat diet (hfd). Sixteen weeks later, the body weight, blood sugar, blood pressure and blood lipid were determined, and aortas were stained with oil red O and hematoxylin to evaluate the AS plaque. \u0000 \u0000 \u0000Results \u0000Cholesterol [(20.09±1.02) mmol/L] and low density lipoprotein cholesterol [(6.84±0.65) mmol/L] of ApoE-/- mice with hfd were significantly increased as compared with that in C57BL/6J normal diet (nd) group [total cholesterol (TC): (2.04±0.07) mmol/L, LDL-C: (0.25±0.01) mmol/L, F=190.543, 82.795, P<0.01]. Oil Red O staining of entire aorta showed that AS lesion size in ApoE-/-+ hfd mice [(22.09±3.49)%] was dramatically increased as compared with that in ApoE-/-+ nd mice [(1.46±0.96)%, F=118.558, P<0.01]. Similar result was obtained from cross-sections of aortic root analysis. Hematoxylin and eosin (HE) staining of cross-sections of aorta root showed typical As plaques. \u0000 \u0000 \u0000Conclusion \u0000The hfd treatment successfully promoted AS development in ApoE-/- mice. The process of gene identification-general situation analysis-blood lipid analysis-morphologic analysis was established to verify AS model. The establishment of mouse AS model provides a valuable tool for the study of AS-related diseases in vivo. \u0000 \u0000 \u0000Key words: \u0000Atherosclerosis; Gene knock out mice; Low density lipoprotein; Cholesterol; Lorta","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"37 1","pages":"172-175"},"PeriodicalIF":0.0,"publicationDate":"2020-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44866914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective To observe the effects of neural stem cells (NSCs) combined with neurotrophin-3 gene modified olfactory ensheathing cells (OECs-NT-3) co-transplants on functional recovery after traumatic brain injury in the adult rats. Methods NSCs and OECs were cultured from hippocampus and olfactory bulb of neonatal rats and then identified. OECs-NT-3 was constructed by lentiviral vector containing NT-3 gene. Male SD rats weighing (200±20) g were randomly divided into sham group, model group, OECs-NT-3 transplantation group, NSCs transplantation group and OECs-NT-3 combined NSCs transplantation group. The rat brain injury model was established. The corresponding cells were transplanted. At day 1, 7, 14 and 28 after transplantation, the modified neurological severity score (mNSS) was used to evaluate neurological function, and brain tissues were taken at each time point for paraffin sections. Hematoxylin-eosin staining was performed. Cell apoptosis was detected by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) method. Immunohistochemical staining of BrdU and p75 was done. Results At day 28 of transplantation, the mNSS scores in rats in the combined group (4.00±1.05) were significantly different from those in the model group (8.50±1.43), the OECs-NT-3 group (5.50±1.35) and the NSCs group (6.00±1.49) (t=-7.997, -2.764, -3.464, P 0.05). Hematoxylin and eosin (HE) staining revealed that the cell density in the sham group, model group, OECs-NT-3 group, NSCs group and the combined group was (220±22), (299±47), (347±35), (390±72) and (523±55) cells, respectively. As compared with the model group, OECs-NT-3 group and NSCs group, the cell density in the combined group was significantly increased (t=7.246, 5.996, 3.373, P<0.05), and the tissue structure was relatively regular. The p75 and BrdU immunohistochemistry showed that the two kinds of transplanted cells could survive continuously and were widely distributed around the lesion. At day 7 after transplantation, the apoptotic index in the sham group, model group, OECs-NT-3 group, NSCs group and combined group was (1.67±0.17)%, (47.49±7.92)%, (31.22±3.97)%, (34.48±4.69)% and (18.17±3.13)% respectively. The apoptosis rate in the combined transplantation group was significantly lower than that in the model group, OECs-NT-3 group and NSCs group (t=5.963, 4.470, 5.012, P<0.05). Conclusion Transplantation of NSCs combined with OECs-NT-3 can alleviate neuronal apoptosis after brain injury in rats, repair tissue defects, and promote the recovery of nerve function. Key words: Neural stem cell; Neurotrophin-3 gene; Gene modify; Olfactory ensheathing cells; Combined transplantation; Traumatic brain injury
{"title":"Effects of neural stem cells in combination with nerve neurotrophic factor 3 gene modified olfactory ensheathing cell co-transplants on functional recovery after traumatic brain injury in the adult rats","authors":"Yaozong Yan, B. Jin, Xin-zhong Zhang, Haiming Li, Wenke Zhou, Dainan Zhang","doi":"10.3760/CMA.J.ISSN.1001-9030.2020.01.021","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2020.01.021","url":null,"abstract":"Objective \u0000To observe the effects of neural stem cells (NSCs) combined with neurotrophin-3 gene modified olfactory ensheathing cells (OECs-NT-3) co-transplants on functional recovery after traumatic brain injury in the adult rats. \u0000 \u0000 \u0000Methods \u0000NSCs and OECs were cultured from hippocampus and olfactory bulb of neonatal rats and then identified. OECs-NT-3 was constructed by lentiviral vector containing NT-3 gene. Male SD rats weighing (200±20) g were randomly divided into sham group, model group, OECs-NT-3 transplantation group, NSCs transplantation group and OECs-NT-3 combined NSCs transplantation group. The rat brain injury model was established. The corresponding cells were transplanted. At day 1, 7, 14 and 28 after transplantation, the modified neurological severity score (mNSS) was used to evaluate neurological function, and brain tissues were taken at each time point for paraffin sections. Hematoxylin-eosin staining was performed. Cell apoptosis was detected by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) method. Immunohistochemical staining of BrdU and p75 was done. \u0000 \u0000 \u0000Results \u0000At day 28 of transplantation, the mNSS scores in rats in the combined group (4.00±1.05) were significantly different from those in the model group (8.50±1.43), the OECs-NT-3 group (5.50±1.35) and the NSCs group (6.00±1.49) (t=-7.997, -2.764, -3.464, P 0.05). Hematoxylin and eosin (HE) staining revealed that the cell density in the sham group, model group, OECs-NT-3 group, NSCs group and the combined group was (220±22), (299±47), (347±35), (390±72) and (523±55) cells, respectively. As compared with the model group, OECs-NT-3 group and NSCs group, the cell density in the combined group was significantly increased (t=7.246, 5.996, 3.373, P<0.05), and the tissue structure was relatively regular. The p75 and BrdU immunohistochemistry showed that the two kinds of transplanted cells could survive continuously and were widely distributed around the lesion. At day 7 after transplantation, the apoptotic index in the sham group, model group, OECs-NT-3 group, NSCs group and combined group was (1.67±0.17)%, (47.49±7.92)%, (31.22±3.97)%, (34.48±4.69)% and (18.17±3.13)% respectively. The apoptosis rate in the combined transplantation group was significantly lower than that in the model group, OECs-NT-3 group and NSCs group (t=5.963, 4.470, 5.012, P<0.05). \u0000 \u0000 \u0000Conclusion \u0000Transplantation of NSCs combined with OECs-NT-3 can alleviate neuronal apoptosis after brain injury in rats, repair tissue defects, and promote the recovery of nerve function. \u0000 \u0000 \u0000Key words: \u0000Neural stem cell; Neurotrophin-3 gene; Gene modify; Olfactory ensheathing cells; Combined transplantation; Traumatic brain injury","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"37 1","pages":"71-74"},"PeriodicalIF":0.0,"publicationDate":"2020-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47615585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-01-08DOI: 10.3760/CMA.J.ISSN.1001-9030.2020.01.036
Z. Hua, Gaopo Cai, Linfeng Zhang, Shirui Liu, Y. Yue, Zhen Li
Objective To analyze the correlation between mitochondrial succinate dehydrogenase (SDH) subunit (A, B, C, D) gene mutations and clinicopathological features of carotid body tumor (CBT) and to explore its prognostic value. Methods Ninety-five patients with sporadic CBT (CBT group) (male 43/female 52), aged 39-70 years old, were all unilateral tumors (55 left/40 right), with tumor diameter of 1.5-10.0 cm. Glenner’s classification was as follows: chemoreceptor tumor in 47 cases, pheochromocytoma in 44 cases, mixed type in 4 cases. The 95 healthy subjects (male 41/female 54), aged 10-69, were selected as the healthy group. PCR was used to amplify the exons of each sub unit gene of SDH and determine the DNA sequence. The gene mutation rate of each sub unit of SDH in CBT group and healthy group was compared. The relationship between the subunits with different mutation rate and the clinicopathological characteristics of the patients and the influence on the prognosis and survival were analyzed, and its predictive value to prognosis was analyzed by logistic regression analysis, and the survival rate of Kaplan Meier was analyzed. Results The mutation rate of SDHB and sDHD in CBT group was 26.32% and 8.84%, respectively. There were no significant differences in the mutation rate of SDHA, SDHC and SDHD between the CBT group and the healthy group (χ2=2.021, 2.212, P>0.05). The mutation rate of SDHB in the CBT group was significantly higher than that in the healthy group (χ2=18.472, P 0.05). The proportion of capsule incompleteness, infiltration of adjacent soft tissue and lymph node metastasis in SDHB mutation group was significantly higher than that in SDHB mutation group (χ2/Z=4.859, 5.566, 9.365, P<0.05). Logistic regression analysis showed that age over 60 years old, incomplete capsule, infiltration of adjacent soft tissue, lymph node metastasis and SDHB mutation were all risk factors for poor prognosis of CBT patients [odds ratio (OR)=2.264, 3.596, 3.117, 3.320, 2.440, P<0.05]. The median follow-up time of 95 patients was 42 months. The 3-year disease-free survival rate of the patients in the non-mutation group and the mutation group was 95.71% and 64.00%, respectively, and the analysis of survival curve showed that the 3-year disease-free survival rate of patients in the non-mutation group of SDHB was significantly higher than that in the mutation group of SDHB (χ2=7.309, P<0.05). Conclusion CBT patients are easy to carry SDHB and SDHD mutation genes. The SDHB mutation gene is closely related to CBT differentiation degree, presence or absence of distant metastasis and prognosis. Key words: Carotid body tumor; Mitochondrial succinate dehydrogenase; Gene mutation; Pathological features; Prognosis
{"title":"Relationship between mitochondrial succinate dehydrogenase gene mutation and clinicopathological features of carotid body tumor and its predictive value for prognosis","authors":"Z. Hua, Gaopo Cai, Linfeng Zhang, Shirui Liu, Y. Yue, Zhen Li","doi":"10.3760/CMA.J.ISSN.1001-9030.2020.01.036","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2020.01.036","url":null,"abstract":"Objective \u0000To analyze the correlation between mitochondrial succinate dehydrogenase (SDH) subunit (A, B, C, D) gene mutations and clinicopathological features of carotid body tumor (CBT) and to explore its prognostic value. \u0000 \u0000 \u0000Methods \u0000Ninety-five patients with sporadic CBT (CBT group) (male 43/female 52), aged 39-70 years old, were all unilateral tumors (55 left/40 right), with tumor diameter of 1.5-10.0 cm. Glenner’s classification was as follows: chemoreceptor tumor in 47 cases, pheochromocytoma in 44 cases, mixed type in 4 cases. The 95 healthy subjects (male 41/female 54), aged 10-69, were selected as the healthy group. PCR was used to amplify the exons of each sub unit gene of SDH and determine the DNA sequence. The gene mutation rate of each sub unit of SDH in CBT group and healthy group was compared. The relationship between the subunits with different mutation rate and the clinicopathological characteristics of the patients and the influence on the prognosis and survival were analyzed, and its predictive value to prognosis was analyzed by logistic regression analysis, and the survival rate of Kaplan Meier was analyzed. \u0000 \u0000 \u0000Results \u0000The mutation rate of SDHB and sDHD in CBT group was 26.32% and 8.84%, respectively. There were no significant differences in the mutation rate of SDHA, SDHC and SDHD between the CBT group and the healthy group (χ2=2.021, 2.212, P>0.05). The mutation rate of SDHB in the CBT group was significantly higher than that in the healthy group (χ2=18.472, P 0.05). The proportion of capsule incompleteness, infiltration of adjacent soft tissue and lymph node metastasis in SDHB mutation group was significantly higher than that in SDHB mutation group (χ2/Z=4.859, 5.566, 9.365, P<0.05). Logistic regression analysis showed that age over 60 years old, incomplete capsule, infiltration of adjacent soft tissue, lymph node metastasis and SDHB mutation were all risk factors for poor prognosis of CBT patients [odds ratio (OR)=2.264, 3.596, 3.117, 3.320, 2.440, P<0.05]. The median follow-up time of 95 patients was 42 months. The 3-year disease-free survival rate of the patients in the non-mutation group and the mutation group was 95.71% and 64.00%, respectively, and the analysis of survival curve showed that the 3-year disease-free survival rate of patients in the non-mutation group of SDHB was significantly higher than that in the mutation group of SDHB (χ2=7.309, P<0.05). \u0000 \u0000 \u0000Conclusion \u0000CBT patients are easy to carry SDHB and SDHD mutation genes. The SDHB mutation gene is closely related to CBT differentiation degree, presence or absence of distant metastasis and prognosis. \u0000 \u0000 \u0000Key words: \u0000Carotid body tumor; Mitochondrial succinate dehydrogenase; Gene mutation; Pathological features; Prognosis","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"37 1","pages":"124-127"},"PeriodicalIF":0.0,"publicationDate":"2020-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44454926","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Objective To explore the relationship between circle microRNA (miRNA, miR)-375 and tissue Yes-associated protein 1 (YAP1) expression in patients with colorectal cancer, as well as their relationship with clinicopathological characteristics of colorectal cancer. Methods Eighty-seven patients with colorectal cancer were selected as the study group, and 80 healthy volunteers served as the control group. The circle miR-375 expression in both groups was detected by quantitative polymerase chain reaction (PCR). The YAP1 expression in both cancer tissue and adjacent healthy tissue was detected by immunohistochemistry. The relationship between the two indexes and clinicopathological characteristics and prognosis was analyzed. The patients in the study group were divided into 3 groups according to miR-375 and YAP1 expression: Lower miR-375 and higher YAP1 (group A, n=21), both lower miR-375 and YAP1, or both higher miR-375 and YAP1 (group B, n=32), and higher miR-375 and lower YAP1 (group C, n=34). The relationship between the two indexes andprognosis was analyzed. Results The circle miR-375 expression in case group (0.132±0.085) was significantly lower than that in the control group (0.521±0.186), and the expression level of YAP1 in cancer tissues (2.201±0.856) was significantly higher than that in healthy tissues (0.814±0.262) (t=51.826, 51.175, P<0.05). There was a linear negative correlation between miR-375 and YAP1 expression (r=-0.691, P<0.05), and the interaction between them was confirmed in double luciferase assay report (t=9.564, P<0.05). The expression of both miR-375 and YAP1 was related to Dukes stage, and the miR-375 expression in patients with colorectal cancer of stage C was significantly lower than that in stage A and stage B, and the YAP1 expression in stage C was significantly higher than that in stage A and stage B (F=4.347, 3.724, P<0.05). The detection of miR-375 combined with YAP1 showed good predictive value for recurrence/metastasis and death of colorectal cancer (AUC=0.739, 0.699, P<0.05). The patients in group A got the shortest median survival time, while the patients in group C got the longest median survival time, and the difference between groups had statistical significance (χ2=4.685, P<0.05). Conclusion There is an interaction between mir-375 and YAP1, and both of them are involved in the occurrence and development of colorectal cancer. Key words: Colorectal cancer; MicroRNA-375; Yes-associated protein 1; Hippo signaling; Prognosis
目的探讨环微小RNA(miRNA,miR)-375与组织Yes-associated protein 1(YAP1)表达的关系及其与癌症临床病理特征的关系。方法选择87例癌症大肠癌患者为研究组,80名健康志愿者为对照组。通过定量聚合酶链式反应(PCR)检测两组中circle miR-375的表达。用免疫组织化学方法检测了YAP1在癌症组织和癌旁健康组织中的表达。分析两项指标与临床病理特征及预后的关系。根据miR-375和YAP1的表达,研究组中的患者被分为3组:较低的miR-375与较高的YAP1(A组,n=21),较低的iR-375与YAP1两者,或较高的miR-37与YAP1二者(B组,n=32),以及较高的miR-375与较低的YAP1两者(C组,n=34)。分析了两项指标与诊断的关系。结果病例组圆圈miR-375的表达(0.132±0.085)显著低于对照组(0.521±0.186),YAP1在癌症组织中的表达水平(2.201±0.856)显著高于健康组织(0.814±0.262)(t=51.826,51.175,P<0.05),二者之间的相互作用在双荧光素酶检测报告中得到证实(t=9.564,P<0.05)。miR-375和YAP1的表达均与Dukes分期有关,C期结直肠癌患者的miR-375表达显著低于A期和B期,C期YAP1表达显著高于A期和B期(F=4.347,3.724,P<0.05)。miR-375联合YAP1检测对癌症复发/转移和死亡具有良好的预测价值(AUC=0.739,0.699,P<0.01),C组患者中位生存时间最长,两组比较差异有统计学意义(x2=4.685,P<0.05)。关键词:结直肠癌癌症;MicroRNA-375;是相关蛋白1;Hippo信号;预后
{"title":"Expression and clinical significance of circulating microRNA-375 and tissue Yes-associated protein 1 in colorectal cancer patients","authors":"Binzhong Zhang, Chun-yan He, Yinda Wang, Lairong Dong","doi":"10.3760/CMA.J.ISSN.1001-9030.2020.01.042","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2020.01.042","url":null,"abstract":"Objective \u0000To explore the relationship between circle microRNA (miRNA, miR)-375 and tissue Yes-associated protein 1 (YAP1) expression in patients with colorectal cancer, as well as their relationship with clinicopathological characteristics of colorectal cancer. \u0000 \u0000 \u0000Methods \u0000Eighty-seven patients with colorectal cancer were selected as the study group, and 80 healthy volunteers served as the control group. The circle miR-375 expression in both groups was detected by quantitative polymerase chain reaction (PCR). The YAP1 expression in both cancer tissue and adjacent healthy tissue was detected by immunohistochemistry. The relationship between the two indexes and clinicopathological characteristics and prognosis was analyzed. The patients in the study group were divided into 3 groups according to miR-375 and YAP1 expression: Lower miR-375 and higher YAP1 (group A, n=21), both lower miR-375 and YAP1, or both higher miR-375 and YAP1 (group B, n=32), and higher miR-375 and lower YAP1 (group C, n=34). The relationship between the two indexes andprognosis was analyzed. \u0000 \u0000 \u0000Results \u0000The circle miR-375 expression in case group (0.132±0.085) was significantly lower than that in the control group (0.521±0.186), and the expression level of YAP1 in cancer tissues (2.201±0.856) was significantly higher than that in healthy tissues (0.814±0.262) (t=51.826, 51.175, P<0.05). There was a linear negative correlation between miR-375 and YAP1 expression (r=-0.691, P<0.05), and the interaction between them was confirmed in double luciferase assay report (t=9.564, P<0.05). The expression of both miR-375 and YAP1 was related to Dukes stage, and the miR-375 expression in patients with colorectal cancer of stage C was significantly lower than that in stage A and stage B, and the YAP1 expression in stage C was significantly higher than that in stage A and stage B (F=4.347, 3.724, P<0.05). The detection of miR-375 combined with YAP1 showed good predictive value for recurrence/metastasis and death of colorectal cancer (AUC=0.739, 0.699, P<0.05). The patients in group A got the shortest median survival time, while the patients in group C got the longest median survival time, and the difference between groups had statistical significance (χ2=4.685, P<0.05). \u0000 \u0000 \u0000Conclusion \u0000There is an interaction between mir-375 and YAP1, and both of them are involved in the occurrence and development of colorectal cancer. \u0000 \u0000 \u0000Key words: \u0000Colorectal cancer; MicroRNA-375; Yes-associated protein 1; Hippo signaling; Prognosis","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"37 1","pages":"144-147"},"PeriodicalIF":0.0,"publicationDate":"2020-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42013434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-01-08DOI: 10.3760/CMA.J.ISSN.1001-9030.2020.01.045
Jialiang Zhou, Haimin Wei, Jia Wu, Q. Fan, Dong-yan Cai
Objective To explore the construction of early warning system for non-small cell lung cancer (NSCLC) by whole genome sequencing. Methods The experiment was divided into two groups: normal tissue and NSCLC tissue. The expression of excision repair cross-complementation group 1 (ERCC1), tubb3 and RRM1 mRNA in NSCLC cells was detected by real-time quantitative reverse transcriptase-polymerase chain reaction (RT-qPCR). The distribution of methylation in NSCLC cells was detected by whole genome sequencing. CpG methylation analysis was performed using sequencing data. Histone modification data were used to analyze the relationship between histone modification and DNA methylation. The expression of histone methylated eggs and methylated related enzymes in normal and NSCLC tissues were detected by protein immunoassay. Results Compared with the control cells, ERCC1 mRNA [(0.78±0.14) vs. (0.12±0.04), χ2=6.370, P<0.05] and RRM1 mRNA [(0.52±0.07) vs. (0.05±0.01), χ2=5.360, P<0.05] expression in NSCLC cells was down-regulated compared with control cells. Methylation level in NSCLC group increased at transcription start site and decreased in intergene region (χ2=3.140, P<0.05). Nine CpG methylation sensitive sites were found in the NSCLC group (RUNX3, MIR196A1, HOXA11, OTP, GATA4, PTPRU, SLC15A3, ZIC1 and TFAP2B). NSCLC group compared with control group, the lower histone acetylation [(H3K9ac [(43.57±8.84) vs. (10.64±4.35), χ2=8.730, P<0.05] and H3K27ac [(40.52±8.64) vs. (9.67±3.58), χ2=5.470, P<0.05) ] and histone methylation [(H2az [(42.56±9.74) vs. (12.47±6.05), χ2=7.420, P<0.05]. H3K4me1 [(37.47±6.42) vs. (15.46±7.34), χ2=5.380, P<0.05], H3K4me2 [(50.37±10.24) vs. (9.47±6.54), χ2=9.270, P<0.05]. H3K4me3 [(52.37±6.49) vs. (10.58±5.88), χ2=1.690, P<0.05] and H3K79me2 [(34.55±6.42) vs. (11.23±6.94), χ2=3.450, P<0.05]. Compared to the control group, NSCLC group DNMT1 express cut [(1.88±0.24) vs. (0.12±0.01), χ2=5.430, P<0.05], DNMT3a expression cut [(1.75±0.36) vs. (0.49±0.11), χ2=7.890, P<0.05], expression of DNMT3b cut [(0.88±0.14) vs. (0.13±0.05), χ2=1.360, P<0.05], expression of H3K4me3 cut [(2.53±0.35) vs. (0.35±0.08), χ2=5.440, P<0.05), H3K9me2 expression cut (0.55±0.07) vs. (0.05±0.01), χ2=3.270, P<0.05]. Conclusion Histone modification is closely related to DNA methylation, and the expression of histone methylation and methylation-related enzymes is also affected. Methylation sensitive sites can be used as biomarkers for early detection of NSCLC. Key words: Whole genome sequencing; Non-small-cell lung carcinoma; Methylation; Histone modification; Lung cancer cells
{"title":"Construction of warning system for lung cancer by whole genome sequencing screening for sensitive methylation sites of non-small-cell lung carcinoma","authors":"Jialiang Zhou, Haimin Wei, Jia Wu, Q. Fan, Dong-yan Cai","doi":"10.3760/CMA.J.ISSN.1001-9030.2020.01.045","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2020.01.045","url":null,"abstract":"Objective \u0000To explore the construction of early warning system for non-small cell lung cancer (NSCLC) by whole genome sequencing. \u0000 \u0000 \u0000Methods \u0000The experiment was divided into two groups: normal tissue and NSCLC tissue. The expression of excision repair cross-complementation group 1 (ERCC1), tubb3 and RRM1 mRNA in NSCLC cells was detected by real-time quantitative reverse transcriptase-polymerase chain reaction (RT-qPCR). The distribution of methylation in NSCLC cells was detected by whole genome sequencing. CpG methylation analysis was performed using sequencing data. Histone modification data were used to analyze the relationship between histone modification and DNA methylation. The expression of histone methylated eggs and methylated related enzymes in normal and NSCLC tissues were detected by protein immunoassay. \u0000 \u0000 \u0000Results \u0000Compared with the control cells, ERCC1 mRNA [(0.78±0.14) vs. (0.12±0.04), χ2=6.370, P<0.05] and RRM1 mRNA [(0.52±0.07) vs. (0.05±0.01), χ2=5.360, P<0.05] expression in NSCLC cells was down-regulated compared with control cells. Methylation level in NSCLC group increased at transcription start site and decreased in intergene region (χ2=3.140, P<0.05). Nine CpG methylation sensitive sites were found in the NSCLC group (RUNX3, MIR196A1, HOXA11, OTP, GATA4, PTPRU, SLC15A3, ZIC1 and TFAP2B). NSCLC group compared with control group, the lower histone acetylation [(H3K9ac [(43.57±8.84) vs. (10.64±4.35), χ2=8.730, P<0.05] and H3K27ac [(40.52±8.64) vs. (9.67±3.58), χ2=5.470, P<0.05) ] and histone methylation [(H2az [(42.56±9.74) vs. (12.47±6.05), χ2=7.420, P<0.05]. H3K4me1 [(37.47±6.42) vs. (15.46±7.34), χ2=5.380, P<0.05], H3K4me2 [(50.37±10.24) vs. (9.47±6.54), χ2=9.270, P<0.05]. H3K4me3 [(52.37±6.49) vs. (10.58±5.88), χ2=1.690, P<0.05] and H3K79me2 [(34.55±6.42) vs. (11.23±6.94), χ2=3.450, P<0.05]. Compared to the control group, NSCLC group DNMT1 express cut [(1.88±0.24) vs. (0.12±0.01), χ2=5.430, P<0.05], DNMT3a expression cut [(1.75±0.36) vs. (0.49±0.11), χ2=7.890, P<0.05], expression of DNMT3b cut [(0.88±0.14) vs. (0.13±0.05), χ2=1.360, P<0.05], expression of H3K4me3 cut [(2.53±0.35) vs. (0.35±0.08), χ2=5.440, P<0.05), H3K9me2 expression cut (0.55±0.07) vs. (0.05±0.01), χ2=3.270, P<0.05]. \u0000 \u0000 \u0000Conclusion \u0000Histone modification is closely related to DNA methylation, and the expression of histone methylation and methylation-related enzymes is also affected. Methylation sensitive sites can be used as biomarkers for early detection of NSCLC. \u0000 \u0000 \u0000Key words: \u0000Whole genome sequencing; Non-small-cell lung carcinoma; Methylation; Histone modification; Lung cancer cells","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"37 1","pages":"155-157"},"PeriodicalIF":0.0,"publicationDate":"2020-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44777653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-01-08DOI: 10.3760/CMA.J.ISSN.1001-9030.2020.01.053
F. Wan, K. Feng, X. Qu, Y. Xia, Haibin Guo, Cuilian Zhang
{"title":"Long non-coding RNA HIT promotes bladder cancer proliferation and invasion by regulating epithelial-mesenchymal transition","authors":"F. Wan, K. Feng, X. Qu, Y. Xia, Haibin Guo, Cuilian Zhang","doi":"10.3760/CMA.J.ISSN.1001-9030.2020.01.053","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2020.01.053","url":null,"abstract":"","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"37 1","pages":"178-179"},"PeriodicalIF":0.0,"publicationDate":"2020-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45618110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-01-08DOI: 10.3760/CMA.J.ISSN.1001-9030.2020.01.060
Zhan Wu, Fudi Zhong, Guandou Yuan, Songqing He
Alcoholic liver disease (ALD) is a major health problem globally. Long-term drinking can lead to fatty liver and inflammation, which in turn may cause liver fibrosis, cirrhosis or liver cancer. At present, the potential mechanism is not fully understood, and growing evidence shows that microRNAs (miRNAs, miR) play an important role in different stages of ALD. In this paper, the research progress in the role of various miRNAs in different stages of ALD is reviewed, and their application in ALD is prospected. Key words: Alcoholic liver disease; MicroRNA; Alcoholic fatty liver; Alcoholic hepatitis; Alcohol hepatic fibrosis
{"title":"Research progress in relationship between microRNAs and alcoholic liver disease","authors":"Zhan Wu, Fudi Zhong, Guandou Yuan, Songqing He","doi":"10.3760/CMA.J.ISSN.1001-9030.2020.01.060","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2020.01.060","url":null,"abstract":"Alcoholic liver disease (ALD) is a major health problem globally. Long-term drinking can lead to fatty liver and inflammation, which in turn may cause liver fibrosis, cirrhosis or liver cancer. At present, the potential mechanism is not fully understood, and growing evidence shows that microRNAs (miRNAs, miR) play an important role in different stages of ALD. In this paper, the research progress in the role of various miRNAs in different stages of ALD is reviewed, and their application in ALD is prospected. \u0000 \u0000Key words: \u0000Alcoholic liver disease; MicroRNA; Alcoholic fatty liver; Alcoholic hepatitis; Alcohol hepatic fibrosis","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"37 1","pages":"194-198"},"PeriodicalIF":0.0,"publicationDate":"2020-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42335360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2020-01-08DOI: 10.3760/CMA.J.ISSN.1001-9030.2020.01.022
Jiwei Li, Quan Zhang, Lei Xu, Zibo Zhu, Saisai Li, Li Wei
Objective To explore the molecular mechanism by which long non-coding RNA (lncRNA) migration inhibitory factor antisense RNA1 (MIF-AS1)/microRNA (miRNAM miR)-370-3p/mitogen activated protein kinase 9 (MAP3K9) molecular axis regulates proliferation, invasion and migration of non-small cell lung cancer (NSCLC). Methods Twenty cancer samples of NSCLC patients were collected from Henan Provincial People’s Hospital from May 2017 to January 2019. There were 12 males and 8 females, aged (52.37±10.34) years. Real-time quantitative reverse transcriptase-polymerase chain reaction (RT-qPCR) and Western blotting were used to detect the expression levels of MIF-AS1, miR-370-3p and MAP3K9 in cancer tissues and 9 cell lines. NSCLC A549 cells were transfected with si-MIF-AS1, si-NC, si-MIF-AS1+ anti-miR-370-3p or si-MIF-AS1+ pcDNA-MAP3K9, respectively. Methyl thiazol tetrazolium (MTT) assay and Transwell assay were used to detect the proliferation, migration and invasion of transfected cells. Western blotting was used to detect the expression of Cyclin D1, p21, p27, matrix metalloproteinase (MMP)-2, MMP-9 and MMP-14 proteins. The dual luciferase reporter gene verified the targeting regulation of MIF-AS1 on miR-370-3p and miR-370-3p on MAP3K9. Results The expression of MIF-AS1 and MAP3K9 in NSCLC tissues (2.49±0.25 and 2.24±0.22) and A549 cells (2.54±0.24 and 2.31±0.23), H1299 cells (2.11±0.21 and 2.44±0.24) and PC-9 cells (2.26±0.23 and 2.16±0.22) was significantly higher than that in adjacent tissues (1.00±0.09 and 1.02±0.09) and normal lung epithelial cells BEAS-2B (1.01±0.09 and 1.00±0.09) (t=25.078, P<0.05; F=94.367, P<0.05). The expression of miR-370-3p in NSCLC tissues (0.42±0.04), A549 cells (0.34±0.03), H1299 cells (0.53±0.05), and PC-9 cells (0.44±0.04) was significantly lower than that in adjacent tissues (1.01±0.08) and BEAS-2B cells (1.00±0.08) (t=29.500, P<0.05; F=269.552, P<0.05). Transfection with si-MIF-AS1 significantly inhibited NSCLC cell proliferation (24 h: 0.27±0.03, 48 h: 0.36±0.03, 72 h: 0.48±0.04), invasion (24.33±3.14), migration (32.46±3.34) ability (P<0.01), up-regulated p21 (0.64±0.06), p27 (0.77±0.07) protein expression (t=17.441, P<0.05; t=17.726, P<0.05) and down-regulated Cyclin D1 (0.29±0.03), MMP-2 (0.25±0.03), MMP-9 (0.34±0.03) and MMP-14 (0.29±0.03) protein expression (t=17.732, P<0.05). The dual luciferase reporter gene confirmed that MIF-AS1 was bond to miR-370-3p and miR-370-3p was bond to MAP3K9. Transfection with si-MIF-AS1+ anti-miR-370-3p or si-MIF-AS1+ pcDNA-MAP3K9 inhibited the effects of si-MIF-AS1 on proliferation, invasion and migration of NSCLC cells. Conclusion LncRNA MIF-AS1 promotes proliferation, migration and invasion of NSCLCs by regulating miR-370-3p/MAP3K9 molecular axis. Key words: Non-small cell lung cancer; Long non-coding RNA migration inhibitory factor antisense RNA1; MicroRNA-370-3p; Mitogen activated protein kinase 9; Proliferation; Migration; Invasion
{"title":"Study on the mechanism of long non-coding RNA migration inhibitory factor antisense RNA1 in regulating proliferation, invasion and metastasis of non-small cell lung cancer","authors":"Jiwei Li, Quan Zhang, Lei Xu, Zibo Zhu, Saisai Li, Li Wei","doi":"10.3760/CMA.J.ISSN.1001-9030.2020.01.022","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2020.01.022","url":null,"abstract":"Objective \u0000To explore the molecular mechanism by which long non-coding RNA (lncRNA) migration inhibitory factor antisense RNA1 (MIF-AS1)/microRNA (miRNAM miR)-370-3p/mitogen activated protein kinase 9 (MAP3K9) molecular axis regulates proliferation, invasion and migration of non-small cell lung cancer (NSCLC). \u0000 \u0000 \u0000Methods \u0000Twenty cancer samples of NSCLC patients were collected from Henan Provincial People’s Hospital from May 2017 to January 2019. There were 12 males and 8 females, aged (52.37±10.34) years. Real-time quantitative reverse transcriptase-polymerase chain reaction (RT-qPCR) and Western blotting were used to detect the expression levels of MIF-AS1, miR-370-3p and MAP3K9 in cancer tissues and 9 cell lines. NSCLC A549 cells were transfected with si-MIF-AS1, si-NC, si-MIF-AS1+ anti-miR-370-3p or si-MIF-AS1+ pcDNA-MAP3K9, respectively. Methyl thiazol tetrazolium (MTT) assay and Transwell assay were used to detect the proliferation, migration and invasion of transfected cells. Western blotting was used to detect the expression of Cyclin D1, p21, p27, matrix metalloproteinase (MMP)-2, MMP-9 and MMP-14 proteins. The dual luciferase reporter gene verified the targeting regulation of MIF-AS1 on miR-370-3p and miR-370-3p on MAP3K9. \u0000 \u0000 \u0000Results \u0000The expression of MIF-AS1 and MAP3K9 in NSCLC tissues (2.49±0.25 and 2.24±0.22) and A549 cells (2.54±0.24 and 2.31±0.23), H1299 cells (2.11±0.21 and 2.44±0.24) and PC-9 cells (2.26±0.23 and 2.16±0.22) was significantly higher than that in adjacent tissues (1.00±0.09 and 1.02±0.09) and normal lung epithelial cells BEAS-2B (1.01±0.09 and 1.00±0.09) (t=25.078, P<0.05; F=94.367, P<0.05). The expression of miR-370-3p in NSCLC tissues (0.42±0.04), A549 cells (0.34±0.03), H1299 cells (0.53±0.05), and PC-9 cells (0.44±0.04) was significantly lower than that in adjacent tissues (1.01±0.08) and BEAS-2B cells (1.00±0.08) (t=29.500, P<0.05; F=269.552, P<0.05). Transfection with si-MIF-AS1 significantly inhibited NSCLC cell proliferation (24 h: 0.27±0.03, 48 h: 0.36±0.03, 72 h: 0.48±0.04), invasion (24.33±3.14), migration (32.46±3.34) ability (P<0.01), up-regulated p21 (0.64±0.06), p27 (0.77±0.07) protein expression (t=17.441, P<0.05; t=17.726, P<0.05) and down-regulated Cyclin D1 (0.29±0.03), MMP-2 (0.25±0.03), MMP-9 (0.34±0.03) and MMP-14 (0.29±0.03) protein expression (t=17.732, P<0.05). The dual luciferase reporter gene confirmed that MIF-AS1 was bond to miR-370-3p and miR-370-3p was bond to MAP3K9. Transfection with si-MIF-AS1+ anti-miR-370-3p or si-MIF-AS1+ pcDNA-MAP3K9 inhibited the effects of si-MIF-AS1 on proliferation, invasion and migration of NSCLC cells. \u0000 \u0000 \u0000Conclusion \u0000LncRNA MIF-AS1 promotes proliferation, migration and invasion of NSCLCs by regulating miR-370-3p/MAP3K9 molecular axis. \u0000 \u0000 \u0000Key words: \u0000Non-small cell lung cancer; Long non-coding RNA migration inhibitory factor antisense RNA1; MicroRNA-370-3p; Mitogen activated protein kinase 9; Proliferation; Migration; Invasion","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"37 1","pages":"75-80"},"PeriodicalIF":0.0,"publicationDate":"2020-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43197891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}