Pub Date : 2020-01-08DOI: 10.3760/CMA.J.ISSN.1001-9030.2020.01.046
Yanwei Zhang, B. Peng, Lin Liu, Feng Ai, Jiayong Zheng, Xiaosong Hu
Objective To observe the levels of aryl hydrocarbon receptor nuclear translocator (ARNT) in lung tissue of children with congenital heart disease (CHD) pulmonary artery hypertension (PAH) and its effect on proliferation and migration of human pulmonary artery smooth muscle cells (HPASMCs), and to investigate the action mechanism of ARNT in the pathogenesis of CHD-PAH. Methods Sixty patients with CHD ventricular septal defect-associated PAH were selected as CHD-PAH group and 60 children with CHD ventricular septal defect without PAH were selected as CHD group (CHD group) in our hospital. There were no significant difference in age and gender between the two groups. HPASMCs were divided into normoxia group and hypoxia group, which were induced by normoxia and hypoxia respectively. HPASMCs were divided into blank control group (BC group), negative control group (NC group) and siR-ARNT group. The cells in the siR-ARNT group were transfected with ARNT-shRNA lentivirus, and those in the NC group were transfected with negative control lentivirus. The cells in the BC group were not transfected. The expression levels of ARNT protein and mRNA in lung tissue and cells were detected by Western blotting and reverse transcription-polymerase chain reaction (RT-PCR). The cell proliferation ability was determined by the cell counting kit-8 (CCK-8) method. Transwell and scratch assays were used to measure cell migration ability. SPSS 20.0 software was used for analysis. The test methods were t test and analysis of variance. Results The expression levels of ARNT protein and mRNA in lung tissue of CHD-PAH group (0.53±0.06 and 2.36±0.17) were significantly higher than those in CHD group (0.09±0.02, 1.00±0.12, t=53.889 and 50.626, P 0.05). Conclusion The ARNT levels in lung tissue of children with CHD-PAH are elevated. ARNT may participate in the development of CHD-PAH by affecting the proliferation and migration of HPASMCs. Key words: Congenital heart disease; Pulmonary hypertension; Aryl hydrocarbon receptor nuclear translocation protein; Pulmonary artery smooth muscle cells; Proliferation; Migration
{"title":"Levels of aryl hydrocarbon receptor nuclear translocator in lung tissue of children with congenital heart disease pulmonary hypertension and its effect on proliferation and migration of pulmonary artery smooth muscle cells","authors":"Yanwei Zhang, B. Peng, Lin Liu, Feng Ai, Jiayong Zheng, Xiaosong Hu","doi":"10.3760/CMA.J.ISSN.1001-9030.2020.01.046","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2020.01.046","url":null,"abstract":"Objective \u0000To observe the levels of aryl hydrocarbon receptor nuclear translocator (ARNT) in lung tissue of children with congenital heart disease (CHD) pulmonary artery hypertension (PAH) and its effect on proliferation and migration of human pulmonary artery smooth muscle cells (HPASMCs), and to investigate the action mechanism of ARNT in the pathogenesis of CHD-PAH. \u0000 \u0000 \u0000Methods \u0000Sixty patients with CHD ventricular septal defect-associated PAH were selected as CHD-PAH group and 60 children with CHD ventricular septal defect without PAH were selected as CHD group (CHD group) in our hospital. There were no significant difference in age and gender between the two groups. HPASMCs were divided into normoxia group and hypoxia group, which were induced by normoxia and hypoxia respectively. HPASMCs were divided into blank control group (BC group), negative control group (NC group) and siR-ARNT group. The cells in the siR-ARNT group were transfected with ARNT-shRNA lentivirus, and those in the NC group were transfected with negative control lentivirus. The cells in the BC group were not transfected. The expression levels of ARNT protein and mRNA in lung tissue and cells were detected by Western blotting and reverse transcription-polymerase chain reaction (RT-PCR). The cell proliferation ability was determined by the cell counting kit-8 (CCK-8) method. Transwell and scratch assays were used to measure cell migration ability. SPSS 20.0 software was used for analysis. The test methods were t test and analysis of variance. \u0000 \u0000 \u0000Results \u0000The expression levels of ARNT protein and mRNA in lung tissue of CHD-PAH group (0.53±0.06 and 2.36±0.17) were significantly higher than those in CHD group (0.09±0.02, 1.00±0.12, t=53.889 and 50.626, P 0.05). \u0000 \u0000 \u0000Conclusion \u0000The ARNT levels in lung tissue of children with CHD-PAH are elevated. ARNT may participate in the development of CHD-PAH by affecting the proliferation and migration of HPASMCs. \u0000 \u0000 \u0000Key words: \u0000Congenital heart disease; Pulmonary hypertension; Aryl hydrocarbon receptor nuclear translocation protein; Pulmonary artery smooth muscle cells; Proliferation; Migration","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"37 1","pages":"158-161"},"PeriodicalIF":0.0,"publicationDate":"2020-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43328970","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.1001-9030.2020.01.052
Yang Shengzhuang, Liang Xiangsen, Yu Sun, Tao Liu, Wenzhou Liu, Lei Xian
{"title":"Implication of plasma methylated transcription factor 21 gene promoter in early clinical diagnosis of lung cancer","authors":"Yang Shengzhuang, Liang Xiangsen, Yu Sun, Tao Liu, Wenzhou Liu, Lei Xian","doi":"10.3760/CMA.J.ISSN.1001-9030.2020.01.052","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2020.01.052","url":null,"abstract":"","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"37 1","pages":"177-177"},"PeriodicalIF":0.0,"publicationDate":"2020-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46892837","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.1001-9030.2020.01.035
Jiancheng Tan, Xinguo Liu, Jinyan Xing, Yongyuan Tian, Hui-Ping Zhao, Dan Yang, Liang Wang
Objective To investigate the effect of RNA binding protein 6 (RBM6) on the proliferation, migration and apoptosis of laryngeal cancer cells. Methods The expression of RBM6 protein was analyzed by Western blotting in 47 cases of laryngeal cancer and adjacent tissues. RBM6 overexpression cell line and control cell line (RBM6 group and control group) were constructed by RBM6 overexpression lentivirus and control lentivirus respectively. The proliferation of two groups was analyzed by cell counting kit-8 (CCK-8). The migration was analyzed in RBM6 group and control group by scratch test. The apoptosis level in RBM6 group and control group was analyzed by flow cytometry. The growth of tumor cells in vivo in RBM6 group and control group was analyzed by allogeneic tumor transplantation. SPSS 13.0 statistical software was used to analyze the measurement data. Mean±SD was used to express the measurement data, and t-test was used to compare between groups. Results As compared with the level of RBM6 protein in adjacent tissues (1.01±0.23), the expression level of RBM6 protein (0.34±0.12) in laryngeal cancer significantly decreased (t=2.913, P<0.05). As compared with the control group, the cell proliferation ability of RBM6 group significantly decreased (F=3.019, P<0.05). As compared with the control group [(84.18±8.32)%], Scratch healing rate in RBM6 group [(30.11±6.89)%] significantly enhanced (t=4.319, P<0.05). As compared with the control group [(35.61±7.01)%], the apoptosis rate in RBM6 group [(5.23±2.12)%] significantly increased (t=2.192, P<0.05). The results showed that the proliferation rate of cells in the control group was significantly higher than that in the RBM6 group (F=2.908, P<0.05). Conclusion RBM6 can inhibit the proliferation and migration of laryngeal cancer cells, and promote the apoptosis of tumor cells. Key words: RNA binding protein 6; Laryngeal cancer; Proliferation; Migration; Apoptosis
{"title":"Effect of RNA binding protein 6 on proliferation, migration and apoptosis of laryngeal cancer cells","authors":"Jiancheng Tan, Xinguo Liu, Jinyan Xing, Yongyuan Tian, Hui-Ping Zhao, Dan Yang, Liang Wang","doi":"10.3760/CMA.J.ISSN.1001-9030.2020.01.035","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2020.01.035","url":null,"abstract":"Objective \u0000To investigate the effect of RNA binding protein 6 (RBM6) on the proliferation, migration and apoptosis of laryngeal cancer cells. \u0000 \u0000 \u0000Methods \u0000The expression of RBM6 protein was analyzed by Western blotting in 47 cases of laryngeal cancer and adjacent tissues. RBM6 overexpression cell line and control cell line (RBM6 group and control group) were constructed by RBM6 overexpression lentivirus and control lentivirus respectively. The proliferation of two groups was analyzed by cell counting kit-8 (CCK-8). The migration was analyzed in RBM6 group and control group by scratch test. The apoptosis level in RBM6 group and control group was analyzed by flow cytometry. The growth of tumor cells in vivo in RBM6 group and control group was analyzed by allogeneic tumor transplantation. SPSS 13.0 statistical software was used to analyze the measurement data. Mean±SD was used to express the measurement data, and t-test was used to compare between groups. \u0000 \u0000 \u0000Results \u0000As compared with the level of RBM6 protein in adjacent tissues (1.01±0.23), the expression level of RBM6 protein (0.34±0.12) in laryngeal cancer significantly decreased (t=2.913, P<0.05). As compared with the control group, the cell proliferation ability of RBM6 group significantly decreased (F=3.019, P<0.05). As compared with the control group [(84.18±8.32)%], Scratch healing rate in RBM6 group [(30.11±6.89)%] significantly enhanced (t=4.319, P<0.05). As compared with the control group [(35.61±7.01)%], the apoptosis rate in RBM6 group [(5.23±2.12)%] significantly increased (t=2.192, P<0.05). The results showed that the proliferation rate of cells in the control group was significantly higher than that in the RBM6 group (F=2.908, P<0.05). \u0000 \u0000 \u0000Conclusion \u0000RBM6 can inhibit the proliferation and migration of laryngeal cancer cells, and promote the apoptosis of tumor cells. \u0000 \u0000 \u0000Key words: \u0000RNA binding protein 6; Laryngeal cancer; Proliferation; Migration; Apoptosis","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"37 1","pages":"121-123"},"PeriodicalIF":0.0,"publicationDate":"2020-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45621571","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 effects of microRNA-155 (miR-155) expression on growth of osteosarcoma cells and the action mechanism. Methods Normal osteoblasts served as the control group and osteosarcoma cells as the experimental group. MiR-155 levels were examined by real-time quantitative polymerase chain reaction (Real-time PCR). The effects of miR-155 on proliferation of osteosarcoma cells and apoptosis were detected by cell counting kit-8 (CCK-8) and flow cytometry assays respectively. Real-time PCR and Western blotting were applied to investigate the target gene of miR-155 in osteosarcoma cells. T test was used for comparison between the two groups, and anova was used for comparison between multiple groups, P<0.05 was considered to be statistically significant. Results MiR-155 expression was significantly up-regulated in osteosarcoma cells (U2OS, Saox-2 and MG-63) (5.10±0.32, 6.82±0.48 and 10.12±0.39) as compared with their matched normal parts (1.01±0.13, t=13.100, P<0.01). CCK-8 indicated that, compared with the negative control group (0.37±0.02, 0.58±0.02, 0.80±0.04), the A values of MG-63 cells were 0.49±0.03, 0.77±0.03, 0.93±0.02, respectively, at 48, 72 and 96 h after transfection with miR-155, and their proliferation capacity was significantly enhanced (t=11.200, P<0.05). Moreover, 48 h after transfeetion, the apoptosis rate of MG-63 cells in miR-155 treatment group was (0.90±0.13)%, significantly lower than in miR-control group [(5.92±0.80)%, t=17.900, P<0.05]. Conclusion Our data revealed that miR-155 may function as an oncogene in osteosarcoma development and it may also provide a therapeutic strategy for controlling osteosarcoma progression. Key words: Osteosarcoma; MicroRNA-155
{"title":"Effect of microRNA-155 on proliferation of osteosarcoma cells in vitro","authors":"Chuangjian Wang, Xiaobo Zhang, Hong-jian Liu, Chunlin Zhang, Xue-ping Wu, Yan Zhang","doi":"10.3760/CMA.J.ISSN.1001-9030.2020.01.032","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2020.01.032","url":null,"abstract":"Objective \u0000To explore the effects of microRNA-155 (miR-155) expression on growth of osteosarcoma cells and the action mechanism. \u0000 \u0000 \u0000Methods \u0000Normal osteoblasts served as the control group and osteosarcoma cells as the experimental group. MiR-155 levels were examined by real-time quantitative polymerase chain reaction (Real-time PCR). The effects of miR-155 on proliferation of osteosarcoma cells and apoptosis were detected by cell counting kit-8 (CCK-8) and flow cytometry assays respectively. Real-time PCR and Western blotting were applied to investigate the target gene of miR-155 in osteosarcoma cells. T test was used for comparison between the two groups, and anova was used for comparison between multiple groups, P<0.05 was considered to be statistically significant. \u0000 \u0000 \u0000Results \u0000MiR-155 expression was significantly up-regulated in osteosarcoma cells (U2OS, Saox-2 and MG-63) (5.10±0.32, 6.82±0.48 and 10.12±0.39) as compared with their matched normal parts (1.01±0.13, t=13.100, P<0.01). CCK-8 indicated that, compared with the negative control group (0.37±0.02, 0.58±0.02, 0.80±0.04), the A values of MG-63 cells were 0.49±0.03, 0.77±0.03, 0.93±0.02, respectively, at 48, 72 and 96 h after transfection with miR-155, and their proliferation capacity was significantly enhanced (t=11.200, P<0.05). Moreover, 48 h after transfeetion, the apoptosis rate of MG-63 cells in miR-155 treatment group was (0.90±0.13)%, significantly lower than in miR-control group [(5.92±0.80)%, t=17.900, P<0.05]. \u0000 \u0000 \u0000Conclusion \u0000Our data revealed that miR-155 may function as an oncogene in osteosarcoma development and it may also provide a therapeutic strategy for controlling osteosarcoma progression. \u0000 \u0000 \u0000Key words: \u0000Osteosarcoma; MicroRNA-155","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"37 1","pages":"112-114"},"PeriodicalIF":0.0,"publicationDate":"2020-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43493922","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.1001-9030.2020.01.001
Mingzhe Li, Yinmo Yang
Pancreatic ductal adenocarcinoma (PDAC) is one of the worst digestive malignancies. The prognosis of this disease remains dismal since the facts that it is difficult to be diagnosed in early stage, has a low rate of surgical resection, and is not sensitive to conventional chemoradiotherapy. Exosomes are a kind of bilayer lipid bodies containing a variety of bioactive molecules, such as proteins, RNA, DNA, lipid, and exist stably in body fluids. As an important component in tumor microenvironment, exosomes are correlated with the malignant phenotype and chemoreistance of pancreatic cancer; as a potential diagnostic biomarker, exosome detection has potential application value in early diagnosis, efficacy evaluation, and tumor recurrence monitoring of pancreatic cancer. Key words: Pancreatic ductal adenocarcinoma; Exosome; Tumor microenvironment; Biomarker
{"title":"Research status and progress of exosomes in pancreatic cancer","authors":"Mingzhe Li, Yinmo Yang","doi":"10.3760/CMA.J.ISSN.1001-9030.2020.01.001","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2020.01.001","url":null,"abstract":"Pancreatic ductal adenocarcinoma (PDAC) is one of the worst digestive malignancies. The prognosis of this disease remains dismal since the facts that it is difficult to be diagnosed in early stage, has a low rate of surgical resection, and is not sensitive to conventional chemoradiotherapy. Exosomes are a kind of bilayer lipid bodies containing a variety of bioactive molecules, such as proteins, RNA, DNA, lipid, and exist stably in body fluids. As an important component in tumor microenvironment, exosomes are correlated with the malignant phenotype and chemoreistance of pancreatic cancer; as a potential diagnostic biomarker, exosome detection has potential application value in early diagnosis, efficacy evaluation, and tumor recurrence monitoring of pancreatic cancer. \u0000 \u0000Key words: \u0000Pancreatic ductal adenocarcinoma; Exosome; Tumor microenvironment; Biomarker","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"37 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2020-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43538782","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.1001-9030.2020.01.004
Z-F Jiao, Yueshan Zhang, Ning-ning Feng, Baoming Yang, Jian-kun Li, Xi Kang, J-W Fu, Heng Cao, Biao Dong, Shunxiang Wang
Objective To explore the effect of microRNA (miRNA, miR)-762 on the drug resistance to gemcitabine (GEM) of pancreatic cancer PANC-1 cells. Methods Real-time quantitative polymerase chain reaction (Real-time PCR) was used to detect the expression of miR-762 mRNA in gemcitabine-resistant pancreatic cancer cell line PANC-1/GEM and the non-drug-resistant cell line PANC-1 of pancreatic cancer. The miR-762 mimics, miR-762 inhibitors and scramble sequences were transfected into PANC-1/GEM cells respectively with Lipofectamine™ 2000. The proliferation and the drug sensitivity of PANC-1/GEM cells to GEM were measured by cell counting kit-8 (CCK-8) assay. The apoptosis of PANC-1/GEM cells was examined by flow cytometry. The expression of apoptosis related proteins was detected by Western blotting. Results The miR-762 expression was significantly up-regulated in PANC-1/GEM cells (2.88±0.37) compared to that in PANC-1 cells (1.22±0.32) (t=7.340, P<0.01), and the difference is statistically significant. The miR-762 mRNA expression in PANC-1/GEM cells were obviously increased after transfection with miR-762 mimics in mimics group (4.96±0.67) as compared with negative control group (2.87±0.45) (t=-4.920, P<0.01), but markedly decreased after transfection with miR-762 inhibitors in mimics group (0.72±0.18) as compared with negative control group (2.87±0.45) (t=8.430, P<0.01). Meanwhile, A450, half maximal inhibitory concentration (IC50) and B cell lymphoma/leukemia-2 (bcl-2), phosphorylated protein kinase B (p-Akt) and phosphorylated glycogen synthase kinase 3β (p-GSK-3β) protein expression in miR-762 mimics group were significantly higher than those in negative control group after transfection, and apoptosis rate and bcl-2 associated X protein (bax) protein expression were significantly lower than those in negative control group after transfection. While A450, IC50 and bcl-2, p-Akt and p-GSK-3β protein expression in miR-762 inhibitors group were significantly lower than those in negative control group after transfection, and apoptosis rate and bax protein expression were significantly higher than those in negative control group after transfection (P<0.01). Conclusion The expression of miR-762 is up-regulated in pancreatic cancer drug resistant cells and can induce the cell proliferation and inhibit cell apoptosis in PANC-1/GEM cells, thus reducing the sensitivity of PANC-1/GEM cells to GEM, which may be associated with the inhibition of pro-apoptotic factor bax expression and the promotion of bcl-2, p-Akt and p-GSK-3β expression. Key words: Pancreatic cancer; MicroRNA-762; Gemcitabine; Chemoresistance
{"title":"Effect of microRNA-762 on the drug resistance to gemcitabine of pancreatic cancer PANC-1 cell line","authors":"Z-F Jiao, Yueshan Zhang, Ning-ning Feng, Baoming Yang, Jian-kun Li, Xi Kang, J-W Fu, Heng Cao, Biao Dong, Shunxiang Wang","doi":"10.3760/CMA.J.ISSN.1001-9030.2020.01.004","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2020.01.004","url":null,"abstract":"Objective \u0000To explore the effect of microRNA (miRNA, miR)-762 on the drug resistance to gemcitabine (GEM) of pancreatic cancer PANC-1 cells. \u0000 \u0000 \u0000Methods \u0000Real-time quantitative polymerase chain reaction (Real-time PCR) was used to detect the expression of miR-762 mRNA in gemcitabine-resistant pancreatic cancer cell line PANC-1/GEM and the non-drug-resistant cell line PANC-1 of pancreatic cancer. The miR-762 mimics, miR-762 inhibitors and scramble sequences were transfected into PANC-1/GEM cells respectively with Lipofectamine™ 2000. The proliferation and the drug sensitivity of PANC-1/GEM cells to GEM were measured by cell counting kit-8 (CCK-8) assay. The apoptosis of PANC-1/GEM cells was examined by flow cytometry. The expression of apoptosis related proteins was detected by Western blotting. \u0000 \u0000 \u0000Results \u0000The miR-762 expression was significantly up-regulated in PANC-1/GEM cells (2.88±0.37) compared to that in PANC-1 cells (1.22±0.32) (t=7.340, P<0.01), and the difference is statistically significant. The miR-762 mRNA expression in PANC-1/GEM cells were obviously increased after transfection with miR-762 mimics in mimics group (4.96±0.67) as compared with negative control group (2.87±0.45) (t=-4.920, P<0.01), but markedly decreased after transfection with miR-762 inhibitors in mimics group (0.72±0.18) as compared with negative control group (2.87±0.45) (t=8.430, P<0.01). Meanwhile, A450, half maximal inhibitory concentration (IC50) and B cell lymphoma/leukemia-2 (bcl-2), phosphorylated protein kinase B (p-Akt) and phosphorylated glycogen synthase kinase 3β (p-GSK-3β) protein expression in miR-762 mimics group were significantly higher than those in negative control group after transfection, and apoptosis rate and bcl-2 associated X protein (bax) protein expression were significantly lower than those in negative control group after transfection. While A450, IC50 and bcl-2, p-Akt and p-GSK-3β protein expression in miR-762 inhibitors group were significantly lower than those in negative control group after transfection, and apoptosis rate and bax protein expression were significantly higher than those in negative control group after transfection (P<0.01). \u0000 \u0000 \u0000Conclusion \u0000The expression of miR-762 is up-regulated in pancreatic cancer drug resistant cells and can induce the cell proliferation and inhibit cell apoptosis in PANC-1/GEM cells, thus reducing the sensitivity of PANC-1/GEM cells to GEM, which may be associated with the inhibition of pro-apoptotic factor bax expression and the promotion of bcl-2, p-Akt and p-GSK-3β expression. \u0000 \u0000 \u0000Key words: \u0000Pancreatic cancer; MicroRNA-762; Gemcitabine; Chemoresistance","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"37 1","pages":"15-18"},"PeriodicalIF":0.0,"publicationDate":"2020-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43360331","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.1001-9030.2020.01.055
Tian Xiangyong, Du Wenjing, W. Xiaoqiang, Chan Zhang, Zhi-wei Wang, G. Cao, T. Yan
{"title":"Role of ciprofloxacin in preemptive therapy of BK viruria in renal transplant recipients","authors":"Tian Xiangyong, Du Wenjing, W. Xiaoqiang, Chan Zhang, Zhi-wei Wang, G. Cao, T. Yan","doi":"10.3760/CMA.J.ISSN.1001-9030.2020.01.055","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2020.01.055","url":null,"abstract":"","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"37 1","pages":"181-181"},"PeriodicalIF":0.0,"publicationDate":"2020-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42322714","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.1001-9030.2020.01.025
Bowen Liu, Peng Li, Chaohui Gu, Zhankui Jia, Jinjian Yang
Objective To establish a mouse model of neurogenic bladder and to investigate the changes of fibronectin 1 (FN1) and the action mechanism of microRNA (miRNA, miR)-1a-3p. Methods Mice were divided into model group and control group. The model group received subcutaneous injection of myelin oligodendrocyte glycoprotein and mycobacterium tuberculosis, and intraperitoneal injection of pertussis toxin at 48 h. The control group received subcutaneous injection of normal saline. The frequency of urination and the amount of urine output were observed. The mice were sacrificed and the bladder tissue was taken. Three bladders were selected from the model group and the control group for high-throughput sequencing. The changes of FN1 and miR-1a-3p in mouse bladder tissues were detected by real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blotting. Results The sequencing results were analyzed. As the urinary system symptoms worsened, FN1 increased (4.569±0.426, t=-5.142, P<0.01), while miR-1a-3p decreased (1.623±0.312, t=-3.945, P<0.05). Compared with the control group, the expression of FN1 mRNA [2.501 (1.301, 4.251), F=99.183, P<0.01] and protein [2.937 (1.174, 4.262), F=63.834, P<0.01] in the bladder tissue of the model group was up-regulated, and that of miR-1a-3p was down-regulated [2.401 (1.250, 3.001), F=35.951, P<0.01]. The dual luciferase gene report indicated that FN1 was a direct target gene of miR-1a-3p (0.514±0.027, t=13.355, P<0.01). Conclusion The animal model of neurogenic bladder has urinary frequency, urgency, urinary retention and other symptoms, and the expression of FN1 is up-regulated, while the expression of miR-1a-3p is down-regulated. Therefore, miR-1a-3p may participate in neurogenic bladder formation through regulation of FN1. Key words: Neurogenic bladder; Fibronectin 1; MicroRNA-1a-3p
{"title":"Action mechanism of microRNA-1a-3p in mouse neurogenic bladder","authors":"Bowen Liu, Peng Li, Chaohui Gu, Zhankui Jia, Jinjian Yang","doi":"10.3760/CMA.J.ISSN.1001-9030.2020.01.025","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2020.01.025","url":null,"abstract":"Objective \u0000To establish a mouse model of neurogenic bladder and to investigate the changes of fibronectin 1 (FN1) and the action mechanism of microRNA (miRNA, miR)-1a-3p. \u0000 \u0000 \u0000Methods \u0000Mice were divided into model group and control group. The model group received subcutaneous injection of myelin oligodendrocyte glycoprotein and mycobacterium tuberculosis, and intraperitoneal injection of pertussis toxin at 48 h. The control group received subcutaneous injection of normal saline. The frequency of urination and the amount of urine output were observed. The mice were sacrificed and the bladder tissue was taken. Three bladders were selected from the model group and the control group for high-throughput sequencing. The changes of FN1 and miR-1a-3p in mouse bladder tissues were detected by real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blotting. \u0000 \u0000 \u0000Results \u0000The sequencing results were analyzed. As the urinary system symptoms worsened, FN1 increased (4.569±0.426, t=-5.142, P<0.01), while miR-1a-3p decreased (1.623±0.312, t=-3.945, P<0.05). Compared with the control group, the expression of FN1 mRNA [2.501 (1.301, 4.251), F=99.183, P<0.01] and protein [2.937 (1.174, 4.262), F=63.834, P<0.01] in the bladder tissue of the model group was up-regulated, and that of miR-1a-3p was down-regulated [2.401 (1.250, 3.001), F=35.951, P<0.01]. The dual luciferase gene report indicated that FN1 was a direct target gene of miR-1a-3p (0.514±0.027, t=13.355, P<0.01). \u0000 \u0000 \u0000Conclusion \u0000The animal model of neurogenic bladder has urinary frequency, urgency, urinary retention and other symptoms, and the expression of FN1 is up-regulated, while the expression of miR-1a-3p is down-regulated. Therefore, miR-1a-3p may participate in neurogenic bladder formation through regulation of FN1. \u0000 \u0000 \u0000Key words: \u0000Neurogenic bladder; Fibronectin 1; MicroRNA-1a-3p","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"37 1","pages":"87-89"},"PeriodicalIF":0.0,"publicationDate":"2020-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48629315","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.1001-9030.2020.01.015
Hongliang Luo, Zhan Wu, Guandou Yuan, Fudi Zhong, Songqing He
Objective To investigate the effect of microRNA-486 (miR-486) on alcoholic fatty liver disease in mice. Methods The progenies of miR-486 knockout mice were obtained by mating of heterozygotes. The 8-week-old progenies were divided into miR-486 knockout control group (KO-PAIR group), miR-486 knockout experimental group (KO-ETOH group), wild type control group (WT-PAIR group) and wild type experimental group (WT-ETOH group), 8 mice in each group. Th mice in experimental group were fed on 5% TP4030D alcohol feed, and those in TP4030C control group were fed on control feed for 4 weeks, 15 ml/mouse per day. On the last day of the experiment, the alcohol group was given alcohol (31.5%) intragastrically, and the control group was administered with dextrin, 100 μl each mouse. After 9 h, the mice were sacrificed and their liver tissues and serum were collected. Liver tissue sections were stained with hematoxylin-eosin (HE) and saturated oil red O. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and tumor necrosis factor-α (TNF-α) were determined. The mRNA and protein expression levels of lipid metabolism related molecules adenosine monophosphate-activated protein kinase (AMPK) and acetyl-coA carboxylase-ser 79 (ACC) were detected by real-time fluorescence quantitative polymerization chain reaction and Western blotting, respectively. The severity of alcoholic fatty liver disease was evaluated and the mechanism was explored. Results HE staining and saturated oil red O staining showed that liver fatification was significantly aggravated in the WT-ETOH group as compared with the KO-ETOH group. As compared with the WT-ETOH group, serum levels of ALT, AST and TNF-α in the KO-ETOH group were significantly reduced [(124.875±38.591) U/L vs. (45.500±20.333) U/L, (190.750±23.789) U/L vs. (140.625±31.794) U/L, and (73.407±17.121) μg/L vs. (50.056±12.717) μg/L, F=32.503, 5.876 and 30.865, P<0.05]. The mRNA level of AMPK in the KO-ETOH group was significantly higher (0.61±0.09 vs. 1.06±0.11, F=21.249, P<0.01), and that of ACC was significantly lower (1.98±0.23 vs. 1.23±0.12, F=68.584, P<0.01) than in the WT-ETOH group, which was further confirmed by Western blotting (0.77±0.09 vs. 1.20±0.08, and 1.16±0.13 vs. 0.38±0.08, P<0.01). Conclusion Deficiency of miR-486 can alleviate alcoholic fatty liver disease in mice probably by regulating lipid metabolism. Key words: MicroRNA-486; Alcoholic fatty liver disease; Lipid metabolism
{"title":"Effect of microRNA-486 on alcoholic fatty liver disease in mice","authors":"Hongliang Luo, Zhan Wu, Guandou Yuan, Fudi Zhong, Songqing He","doi":"10.3760/CMA.J.ISSN.1001-9030.2020.01.015","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2020.01.015","url":null,"abstract":"Objective \u0000To investigate the effect of microRNA-486 (miR-486) on alcoholic fatty liver disease in mice. \u0000 \u0000 \u0000Methods \u0000The progenies of miR-486 knockout mice were obtained by mating of heterozygotes. The 8-week-old progenies were divided into miR-486 knockout control group (KO-PAIR group), miR-486 knockout experimental group (KO-ETOH group), wild type control group (WT-PAIR group) and wild type experimental group (WT-ETOH group), 8 mice in each group. Th mice in experimental group were fed on 5% TP4030D alcohol feed, and those in TP4030C control group were fed on control feed for 4 weeks, 15 ml/mouse per day. On the last day of the experiment, the alcohol group was given alcohol (31.5%) intragastrically, and the control group was administered with dextrin, 100 μl each mouse. After 9 h, the mice were sacrificed and their liver tissues and serum were collected. Liver tissue sections were stained with hematoxylin-eosin (HE) and saturated oil red O. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and tumor necrosis factor-α (TNF-α) were determined. The mRNA and protein expression levels of lipid metabolism related molecules adenosine monophosphate-activated protein kinase (AMPK) and acetyl-coA carboxylase-ser 79 (ACC) were detected by real-time fluorescence quantitative polymerization chain reaction and Western blotting, respectively. The severity of alcoholic fatty liver disease was evaluated and the mechanism was explored. \u0000 \u0000 \u0000Results \u0000HE staining and saturated oil red O staining showed that liver fatification was significantly aggravated in the WT-ETOH group as compared with the KO-ETOH group. As compared with the WT-ETOH group, serum levels of ALT, AST and TNF-α in the KO-ETOH group were significantly reduced [(124.875±38.591) U/L vs. (45.500±20.333) U/L, (190.750±23.789) U/L vs. (140.625±31.794) U/L, and (73.407±17.121) μg/L vs. (50.056±12.717) μg/L, F=32.503, 5.876 and 30.865, P<0.05]. The mRNA level of AMPK in the KO-ETOH group was significantly higher (0.61±0.09 vs. 1.06±0.11, F=21.249, P<0.01), and that of ACC was significantly lower (1.98±0.23 vs. 1.23±0.12, F=68.584, P<0.01) than in the WT-ETOH group, which was further confirmed by Western blotting (0.77±0.09 vs. 1.20±0.08, and 1.16±0.13 vs. 0.38±0.08, P<0.01). \u0000 \u0000 \u0000Conclusion \u0000Deficiency of miR-486 can alleviate alcoholic fatty liver disease in mice probably by regulating lipid metabolism. \u0000 \u0000 \u0000Key words: \u0000MicroRNA-486; Alcoholic fatty liver disease; Lipid metabolism","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"37 1","pages":"52-55"},"PeriodicalIF":0.0,"publicationDate":"2020-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43052040","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.1001-9030.2020.01.018
Xu Jizhong, Gui-xian Wang, W. Yuan, Quanbo Zhou, Shengyun Hu
Objective To observe the effect of microRNA (miRNA, miR)-182 on the proliferation and migration of colorectal cancer cells by targeting special AT-rich sequence-binding protein 2 (SATB2) gene, and to explore its effect on SATB2/icotinamide adenine dinucleotide phosphate oxidase 4 (nox4) pathway. Methods HT-29 cells in logarithmic phase were transfected with Si-miR-182 and Control-si resectively, by liposome transfection, serving as Si-miR-182 group and N-miR-182 group, respectively. The expression of miR-182 gene, the cell proliferation and migration, the mRNA and protein expression of SATB2, nox4, E-cadherin and vimentin were examined. Results The relative expression of miR-182 gene in Si-miR-182 group (0.35±0.05) was lower than that in control group (1.24±0.26) and N-miR-182 group (1.20±0.25) (t=7.517, 7.455, P<0.05). The A values of methyl thiazol tetrazolium (MTT) test in Si-miR-182 group were lower than those in control group and N-miR-182 group after 24, 48 and 72 h of culture (24 h: t=2.667, 2.664; 48 h: t=4.559, 4.524; 72 h: t=7.257, 6.981; P<0.05). Compared with 24-h culture, the A value of MTT test in 48 and 72 hours in three groups were increased (48 h: t=5.507, 5.092, 3.741; 72 h: t=11.330, 10.637, 9.229; P<0.05), and the A value of MTT test in 72 hours were higher than those in 48 hours(t=7.411, 6.941, 5.214, P<0.05). The cell migration rate of Si-miR-182 group [(53.90±3.19)%] was lower than that of the control group [(81.66±5.92)%] and N-miR-182 group [(80.35±5.40)%] (t=9.231, 9.430, P<0.05). The relative expressions of SATB2, E-cadherin mRNA and protein in Si-miR-182 group were higher than those in control group and N-miR-182 group (SATB2: t=10.930, 11.158; E-Cadherin: t=9.288, 9.369; P<0.05), while the relative expressions of nox4, vimentin mRNA and protein in Si-miR-182 group were lower than those in control group and N-miR-182 group (nox4: t=8.955, 7.590; Vimentin: t=6.543, 6.644; P<0.05). Conclusion Silencing of miR-182 gene can significantly inhibit the proliferation and migration of colorectal cancer cells, possibly by activating SATB2, E-Cadherin expression, inhibiting the expression of nox4, Vimentin, and participating in the SATB2/nox4 pathway. Key words: MicroRNA-182; Special AT-rich sequence-binding protein 2; Colorectal cancer; Proliferation; Migration
{"title":"MicroRNA-182 regulates colon cancer cell proliferation and migration by targeting special AT-rich sequence-binding protein 2 gene","authors":"Xu Jizhong, Gui-xian Wang, W. Yuan, Quanbo Zhou, Shengyun Hu","doi":"10.3760/CMA.J.ISSN.1001-9030.2020.01.018","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2020.01.018","url":null,"abstract":"Objective \u0000To observe the effect of microRNA (miRNA, miR)-182 on the proliferation and migration of colorectal cancer cells by targeting special AT-rich sequence-binding protein 2 (SATB2) gene, and to explore its effect on SATB2/icotinamide adenine dinucleotide phosphate oxidase 4 (nox4) pathway. \u0000 \u0000 \u0000Methods \u0000HT-29 cells in logarithmic phase were transfected with Si-miR-182 and Control-si resectively, by liposome transfection, serving as Si-miR-182 group and N-miR-182 group, respectively. The expression of miR-182 gene, the cell proliferation and migration, the mRNA and protein expression of SATB2, nox4, E-cadherin and vimentin were examined. \u0000 \u0000 \u0000Results \u0000The relative expression of miR-182 gene in Si-miR-182 group (0.35±0.05) was lower than that in control group (1.24±0.26) and N-miR-182 group (1.20±0.25) (t=7.517, 7.455, P<0.05). The A values of methyl thiazol tetrazolium (MTT) test in Si-miR-182 group were lower than those in control group and N-miR-182 group after 24, 48 and 72 h of culture (24 h: t=2.667, 2.664; 48 h: t=4.559, 4.524; 72 h: t=7.257, 6.981; P<0.05). Compared with 24-h culture, the A value of MTT test in 48 and 72 hours in three groups were increased (48 h: t=5.507, 5.092, 3.741; 72 h: t=11.330, 10.637, 9.229; P<0.05), and the A value of MTT test in 72 hours were higher than those in 48 hours(t=7.411, 6.941, 5.214, P<0.05). The cell migration rate of Si-miR-182 group [(53.90±3.19)%] was lower than that of the control group [(81.66±5.92)%] and N-miR-182 group [(80.35±5.40)%] (t=9.231, 9.430, P<0.05). The relative expressions of SATB2, E-cadherin mRNA and protein in Si-miR-182 group were higher than those in control group and N-miR-182 group (SATB2: t=10.930, 11.158; E-Cadherin: t=9.288, 9.369; P<0.05), while the relative expressions of nox4, vimentin mRNA and protein in Si-miR-182 group were lower than those in control group and N-miR-182 group (nox4: t=8.955, 7.590; Vimentin: t=6.543, 6.644; P<0.05). \u0000 \u0000 \u0000Conclusion \u0000Silencing of miR-182 gene can significantly inhibit the proliferation and migration of colorectal cancer cells, possibly by activating SATB2, E-Cadherin expression, inhibiting the expression of nox4, Vimentin, and participating in the SATB2/nox4 pathway. \u0000 \u0000 \u0000Key words: \u0000MicroRNA-182; Special AT-rich sequence-binding protein 2; Colorectal cancer; Proliferation; Migration","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"37 1","pages":"63-66"},"PeriodicalIF":0.0,"publicationDate":"2020-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44319666","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}
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