Pub Date : 2019-12-08DOI: 10.3760/CMA.J.ISSN.1001-9030.2019.12.023
Zhenlin Hou, Guihua Wang, Junbo Hu, Jing Wang, Li Sun
Objective To investigate the mechanism of microRNA (miRNA, miR)-29b regulation of tribbles pseudokinase 2 (TRIB2) in colorectal tumors. Methods The online database was used to analyze the miRNAs that bind to the 3’Untranslated Region (UTR) of TRIB2, and the highest scored miR-29b was selected for study. The eukaryotic cell transfection technique was used to interfere with the expression of miR-29b in colorectal tumor cells; Western blotting and real-time quantitative polymerase chain reaction (Real-time PCR) was used to detect the difference in protein and mRNA expression of TRIB2; the position of miR-29b binding on TRIB2-3’untranslated regions (3’UTR) was confirmed by luciferase reporter gene assay; β-galactosidase staining was used to detect effects of miR-29b on colorectal cancer cell senescence. All data were quantified as Mean±SD. Two-tailed Student’s t-test was used to evaluate the differences between two groups. All statistical analyses were performed using SPSS 24.0 (SPSS Inc.). Results In SW48 and SW480 cell lines overexpressing miR-29b, the mRNA levels of TRIB2 decreased to (63.468±4.154)% and (43.145±7.523)% (t=5.351, P 0.05). In the cancer cells overexpressing of miR-29b, the proportion of senescent cells increased from 41.473% to 62.085% (χ2=19.731, P<0.01), and overexpression of TRIB2 reduced the proportion to 46.866% (χ2=12.031, P<0.01). Conclusion miR-29b can inhibits TRIB2 expression and promote the senescence of colorectal tumors, and it can be used as a potential therapeutic target for colorectal cancer. Key words: MicroRNA-29b; Tribbles pseudokinase 2; Colorectal cancer; Cell senescence
{"title":"MicroRNA-29b promotes cellular senescence of colorectal tumors by targeting tribbles pseudokinase 2","authors":"Zhenlin Hou, Guihua Wang, Junbo Hu, Jing Wang, Li Sun","doi":"10.3760/CMA.J.ISSN.1001-9030.2019.12.023","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2019.12.023","url":null,"abstract":"Objective \u0000To investigate the mechanism of microRNA (miRNA, miR)-29b regulation of tribbles pseudokinase 2 (TRIB2) in colorectal tumors. \u0000 \u0000 \u0000Methods \u0000The online database was used to analyze the miRNAs that bind to the 3’Untranslated Region (UTR) of TRIB2, and the highest scored miR-29b was selected for study. The eukaryotic cell transfection technique was used to interfere with the expression of miR-29b in colorectal tumor cells; Western blotting and real-time quantitative polymerase chain reaction (Real-time PCR) was used to detect the difference in protein and mRNA expression of TRIB2; the position of miR-29b binding on TRIB2-3’untranslated regions (3’UTR) was confirmed by luciferase reporter gene assay; β-galactosidase staining was used to detect effects of miR-29b on colorectal cancer cell senescence. All data were quantified as Mean±SD. Two-tailed Student’s t-test was used to evaluate the differences between two groups. All statistical analyses were performed using SPSS 24.0 (SPSS Inc.). \u0000 \u0000 \u0000Results \u0000In SW48 and SW480 cell lines overexpressing miR-29b, the mRNA levels of TRIB2 decreased to (63.468±4.154)% and (43.145±7.523)% (t=5.351, P 0.05). In the cancer cells overexpressing of miR-29b, the proportion of senescent cells increased from 41.473% to 62.085% (χ2=19.731, P<0.01), and overexpression of TRIB2 reduced the proportion to 46.866% (χ2=12.031, P<0.01). \u0000 \u0000 \u0000Conclusion \u0000miR-29b can inhibits TRIB2 expression and promote the senescence of colorectal tumors, and it can be used as a potential therapeutic target for colorectal cancer. \u0000 \u0000 \u0000Key words: \u0000MicroRNA-29b; Tribbles pseudokinase 2; Colorectal cancer; Cell senescence","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"36 1","pages":"2203-2206"},"PeriodicalIF":0.0,"publicationDate":"2019-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44893828","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 study the Expression of anoctamin 7 (ANO7) in the nuclear factor kappa B (NF-κB) signal pathway and its clinical significance in prostate cancer. Methods NF-κB signal pathway activated cell and animal model were constructed using tribbles homolog1 (TRIB1) overexpressed prostate cancer cell line. NF-κB signal pathway inhibited cell model was constructed using NF-κB signal pathway inhibitor. Western blotting and real-time quantitative polymerase chain reaction (Real-time PCR) and immunohistochemistry (IHC) were used to analyze the effect of NF-κB signal pathway on the regulation of ANO7 expression and the relationship between ANO7 expression and clinicopathological features in prostate cancer. Results ANO7 expression was up-regulated in the NF-κB signal pathway-activated cell and animal models. ANO7 expression was down-regulated in the NF-κB signal pathway-inhibited cell models. The high expression level of ANO7 was 45.8% in tumor tissues compared with 85.7% in adjacent non-cancerous tissues, with statistical significance (χ2=7.258, P<0.01). The expression of ANO7 was significantly correlated with Gleason score and pathological grade (χ2=19.797, 19.797, P<0.01). Similar results were obtained from The Cancer Genome Atlas (TCGA) and the Taylor database. Kaplan-Meier analysis found that ANO7 was significantly associated with the patients’prognosis in the Taylor database (P<0.01). Multivariate analysis found that ANO7 (P<0.05), Gleason score (P<0.01) and pathological grade (P<0.01) were independent predictors of prostate cancer using the Cox regression model in the cohort affecting prostate cancer prognosis. Conclusion NF-κB signal pathway regulates ANO7 expression in prostate cancer and the expression of ANO7 is closely related to prostate cancer. Key words: Anoctamin 7; Nuclear factor kappa B signal pathway; Prostate cancer; Prognosis
{"title":"Expression of anoctamin 7 in nuclear factor kappa B signal pathway and its clinical significance in prostate cancer","authors":"Yong Luo, Guian Zhang, Xuejin Zhu, Ren Liu, Wanxiang You, Q. Qian, Xiaoming Xu, Ren-Qiang He, Weide Zhong","doi":"10.3760/CMA.J.ISSN.1001-9030.2019.12.003","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2019.12.003","url":null,"abstract":"Objective \u0000To study the Expression of anoctamin 7 (ANO7) in the nuclear factor kappa B (NF-κB) signal pathway and its clinical significance in prostate cancer. \u0000 \u0000 \u0000Methods \u0000NF-κB signal pathway activated cell and animal model were constructed using tribbles homolog1 (TRIB1) overexpressed prostate cancer cell line. NF-κB signal pathway inhibited cell model was constructed using NF-κB signal pathway inhibitor. Western blotting and real-time quantitative polymerase chain reaction (Real-time PCR) and immunohistochemistry (IHC) were used to analyze the effect of NF-κB signal pathway on the regulation of ANO7 expression and the relationship between ANO7 expression and clinicopathological features in prostate cancer. \u0000 \u0000 \u0000Results \u0000ANO7 expression was up-regulated in the NF-κB signal pathway-activated cell and animal models. ANO7 expression was down-regulated in the NF-κB signal pathway-inhibited cell models. The high expression level of ANO7 was 45.8% in tumor tissues compared with 85.7% in adjacent non-cancerous tissues, with statistical significance (χ2=7.258, P<0.01). The expression of ANO7 was significantly correlated with Gleason score and pathological grade (χ2=19.797, 19.797, P<0.01). Similar results were obtained from The Cancer Genome Atlas (TCGA) and the Taylor database. Kaplan-Meier analysis found that ANO7 was significantly associated with the patients’prognosis in the Taylor database (P<0.01). Multivariate analysis found that ANO7 (P<0.05), Gleason score (P<0.01) and pathological grade (P<0.01) were independent predictors of prostate cancer using the Cox regression model in the cohort affecting prostate cancer prognosis. \u0000 \u0000 \u0000Conclusion \u0000NF-κB signal pathway regulates ANO7 expression in prostate cancer and the expression of ANO7 is closely related to prostate cancer. \u0000 \u0000 \u0000Key words: \u0000Anoctamin 7; Nuclear factor kappa B signal pathway; Prostate cancer; Prognosis","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"36 1","pages":"2137-2140"},"PeriodicalIF":0.0,"publicationDate":"2019-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46424174","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 : 2019-12-08DOI: 10.3760/CMA.J.ISSN.1001-9030.2019.12.056
Ya Xu, Jing Liu
Recent researches demonstrated that N6-methyladenosine (m6A) is one of the most common internal modification of RNA in eukaryotic organisms. This is a dynamic and reversible modification, requiring methyltransferase-like 3 (METTL3)/methyltransferase-like14 (METTL14), fat mass and obesity-associated protein (FTO)/alk B homolog 5(ALKBH5), and YTH domain-containing proteins. The m6A modification of RNA influenced the downstream pathways, through regulating RNA degradation, mircoRNA (miRNA) processing, or translation. Recent emerging studies suggested that m6A was involved in the development and progression of multiple cancers. This article reviewed the expression pattern of m6A in solid tumors and the underlying mechanisms, in order for better understanding the tumorigenesis and development of human tumors and providing potential therapeutic strategies. Key words: N6-methyladenosine; Cancer; Methyltransferase; Demethylases; N6-methyladenosine-binding proteins
{"title":"Current researches on N6-methyladenosine and its functions in solid tumors","authors":"Ya Xu, Jing Liu","doi":"10.3760/CMA.J.ISSN.1001-9030.2019.12.056","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2019.12.056","url":null,"abstract":"Recent researches demonstrated that N6-methyladenosine (m6A) is one of the most common internal modification of RNA in eukaryotic organisms. This is a dynamic and reversible modification, requiring methyltransferase-like 3 (METTL3)/methyltransferase-like14 (METTL14), fat mass and obesity-associated protein (FTO)/alk B homolog 5(ALKBH5), and YTH domain-containing proteins. The m6A modification of RNA influenced the downstream pathways, through regulating RNA degradation, mircoRNA (miRNA) processing, or translation. Recent emerging studies suggested that m6A was involved in the development and progression of multiple cancers. This article reviewed the expression pattern of m6A in solid tumors and the underlying mechanisms, in order for better understanding the tumorigenesis and development of human tumors and providing potential therapeutic strategies. \u0000 \u0000 \u0000Key words: \u0000N6-methyladenosine; Cancer; Methyltransferase; Demethylases; N6-methyladenosine-binding proteins","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"36 1","pages":"2302-2305"},"PeriodicalIF":0.0,"publicationDate":"2019-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"46964800","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 : 2019-12-08DOI: 10.3760/CMA.J.ISSN.1001-9030.2019.12.009
Luo Yang, Gu Chaohui, Y. Rui, Yu Shunli, Zhao Keyuan, Fan Ruixin, Dou Chenyang, Zhang Shaopeng
Objective To investigate the expression level of kinesin superfamily proteins 18A (KIF18A) in bladder cancer tissues and its correlation with clinicopathological features. Methods The clinical data, bladder cancer tissues and adjacent normal tissues samples of 63 patients who underwent radical cystectomy in our hospital from October 2016 to December 2018 were collected. To the normal tissue of the cancer side as a control, to detect the level of KIF18A expression in bladder cancer tissue, according to staining results, bladder cancer patients were divided into KIF18A low expression group and KIF18A high expression group, using the chi-square test or Fisher precision test to compare the clinical and pathological characteristics between the groups, Analysis of the correlation between the degree of expression of KIF18A in bladder cancer tissue and clinical pathological characteristics. Results The high expression rate of KIF18A in bladder cancer tissues was 55.6% (35/63) and the low expression rate was 44.4% (28/63). The high expression rate of KIF18A in normal tissues was 28.6% (18/63) and the low expression rate was 71.4% (45/63). KIF18A expression in bladder cancer was significantly different from that in adjacent normal tissues (χ2=9.412, P 0.05), age (χ2=0.268, P>0.05), the tumor diameter (χ2=0.121, P>0.05), N staging (lymph node involvement staging χ2=4.882, P>0.05), M staging (distant metastasis staging χ2=1.690, P>0.05). T staging (tumor invasion staging χ2=9.264, P<0.05) and pathological grading (χ2=5.119, P<0.05) was significantly related to the high expression rate of KIF18A. Conclusion KIF18A is up-regulated in bladder cancer, and its high expression is positively correlated with T stage and pathological grade. Key words: Bladder cancer; Kinesin superfamily proteins; Kinesin superfamily proteins 18A; Clinicopathologic features
{"title":"The expression and clinical significance of kinesin superfamily proteins 18A in bladder cancer tissues","authors":"Luo Yang, Gu Chaohui, Y. Rui, Yu Shunli, Zhao Keyuan, Fan Ruixin, Dou Chenyang, Zhang Shaopeng","doi":"10.3760/CMA.J.ISSN.1001-9030.2019.12.009","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2019.12.009","url":null,"abstract":"Objective \u0000To investigate the expression level of kinesin superfamily proteins 18A (KIF18A) in bladder cancer tissues and its correlation with clinicopathological features. \u0000 \u0000 \u0000Methods \u0000The clinical data, bladder cancer tissues and adjacent normal tissues samples of 63 patients who underwent radical cystectomy in our hospital from October 2016 to December 2018 were collected. To the normal tissue of the cancer side as a control, to detect the level of KIF18A expression in bladder cancer tissue, according to staining results, bladder cancer patients were divided into KIF18A low expression group and KIF18A high expression group, using the chi-square test or Fisher precision test to compare the clinical and pathological characteristics between the groups, Analysis of the correlation between the degree of expression of KIF18A in bladder cancer tissue and clinical pathological characteristics. \u0000 \u0000 \u0000Results \u0000The high expression rate of KIF18A in bladder cancer tissues was 55.6% (35/63) and the low expression rate was 44.4% (28/63). The high expression rate of KIF18A in normal tissues was 28.6% (18/63) and the low expression rate was 71.4% (45/63). KIF18A expression in bladder cancer was significantly different from that in adjacent normal tissues (χ2=9.412, P 0.05), age (χ2=0.268, P>0.05), the tumor diameter (χ2=0.121, P>0.05), N staging (lymph node involvement staging χ2=4.882, P>0.05), M staging (distant metastasis staging χ2=1.690, P>0.05). T staging (tumor invasion staging χ2=9.264, P<0.05) and pathological grading (χ2=5.119, P<0.05) was significantly related to the high expression rate of KIF18A. \u0000 \u0000 \u0000Conclusion \u0000KIF18A is up-regulated in bladder cancer, and its high expression is positively correlated with T stage and pathological grade. \u0000 \u0000 \u0000Key words: \u0000Bladder cancer; Kinesin superfamily proteins; Kinesin superfamily proteins 18A; Clinicopathologic features","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"36 1","pages":"2157-2159"},"PeriodicalIF":0.0,"publicationDate":"2019-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45321099","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 : 2019-12-08DOI: 10.3760/CMA.J.ISSN.1001-9030.2019.12.014
Weilin Wang, Haib Wango, Runze Zhang, Xiao Wang, Jin Wang, Meisui Lin, Chengqin Wang
Objective To study the effects of KIF3A silencing and overexpression on tumor proliferation, migration and invasion in human triple negative breast cancer (TNBC) cell lines. Methods With lentivirus-mediated interference technology made KIF3A gene silence in TNBC MDA-MB-231 cells, KIF3A gene was transfected into TNBC MDA-MB-468 cells bv liposome method. Subsequently, Western blotting analysis was performed to detect protein expression of KIF3A in these cells. Colony-formation assay, transwell migration and invasion assay were applied to estimate proliferation, migration and invasion ability of cells. Results The expression of KIF3A protein in the KIF3A-shRNA group cells was significantly silenced compared with those in the Scr-shRNA group cells. The expression of KIF3A in the KIF3A-pEX group cells was increased compared with those in the Vector group cells. The colony numbers in the KIF3A-shRNA group were significantly lower than those in Scr-shRNA group (174.8±46.26 vs. 293.2±20.93, P<0.01). The colony numbers in the KIF3A-pEX group were significantly higher than those in Vector group cells (292.00±75.59 vs. 151.40±68.58, P<0.05). The result of the transwell migrated assay showed that the numbers of migrated cells in the KIF3A-shRNA group were significantly lower than those in Scr-shRNA group (47.60±5.77 vs. 161.40±20.16, P<0.01) and the numbers of migrated cells in the KIF3A-pEX group were significantly higher than those in Vector group (262.00±23.35 vs. 155.00±29.15, P<0.01). It was confirmed via the transwell invasion assay results that the cell’s invasive ability of KIF3A-shRNA group was progressively suppressed as compared with the Scr-shRNA group (161.40±16.16 vs. 281.00±19.77, P<0.01) and the cell’s invasive ability of KIF3A-pEX group was progressively promoted as compared with the Vector group (214.00±34.54 vs. 125.40±19.94, P<0.01). Conclusion Down-regulation of KIF3A in TNBC cell can inhibit the cell proliferation, migration and invasion. Overexpression of KIF3A in TNBC cell can promote the cell proliferation, migration and invasion. KIF3A might hold potential as a therapeutic drug target for human TNBC. Key words: KIF3A; Short hairpin RNA; Triple negative breast cancer; Proliferation; Migration; Invasion
目的研究KIF3A沉默和过表达对人三阴性乳腺癌(TNBC)细胞系肿瘤增殖、迁移和侵袭的影响。方法采用慢病毒介导干扰技术使KIF3A基因沉默TNBC MDA-MB-231细胞，脂质体法将KIF3A基因转染TNBC MDA-MB-468细胞。随后，采用Western blotting分析检测KIF3A蛋白在这些细胞中的表达。采用菌落形成试验、跨井迁移和侵袭试验评估细胞的增殖、迁移和侵袭能力。结果与Scr-shRNA组细胞相比，KIF3A蛋白在KIF3A- shrna组细胞中表达明显沉默。与Vector组细胞相比，KIF3A- pex组细胞中KIF3A的表达增加。KIF3A-shRNA组的菌落数显著低于Scr-shRNA组(174.8±46.26 vs 293.2±20.93,P<0.01)。kif3 - pex组细胞集落数显著高于Vector组(292.00±75.59 vs. 151.40±68.58,P<0.05)。transwell迁移实验结果显示，kif3 - shrna组的迁移细胞数显著低于Scr-shRNA组(47.60±5.77 vs. 161.40±20.16,P<0.01)， kif3 - pex组的迁移细胞数显著高于Vector组(262.00±23.35 vs. 155.00±29.15,P<0.01)。跨井侵袭实验结果证实，与Scr-shRNA组相比，kif3 - shrna组细胞的侵袭能力被逐渐抑制(161.40±16.16比281.00±19.77,P<0.01);与Vector组相比，kif3 - pex组细胞的侵袭能力被逐渐增强(214.00±34.54比125.40±19.94,P<0.01)。结论下调KIF3A可抑制TNBC细胞的增殖、迁移和侵袭。KIF3A在TNBC细胞中过表达可促进细胞增殖、迁移和侵袭。KIF3A可能具有作为人类TNBC治疗药物靶点的潜力。关键词:KIF3A;短发夹RNA;三阴性乳腺癌;扩散;迁移;入侵
{"title":"Effects of KIF3A gene silencing and overexpression on proliferation, migration and invasion of human triple negative breast cancer cells","authors":"Weilin Wang, Haib Wango, Runze Zhang, Xiao Wang, Jin Wang, Meisui Lin, Chengqin Wang","doi":"10.3760/CMA.J.ISSN.1001-9030.2019.12.014","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2019.12.014","url":null,"abstract":"Objective \u0000To study the effects of KIF3A silencing and overexpression on tumor proliferation, migration and invasion in human triple negative breast cancer (TNBC) cell lines. \u0000 \u0000 \u0000Methods \u0000With lentivirus-mediated interference technology made KIF3A gene silence in TNBC MDA-MB-231 cells, KIF3A gene was transfected into TNBC MDA-MB-468 cells bv liposome method. Subsequently, Western blotting analysis was performed to detect protein expression of KIF3A in these cells. Colony-formation assay, transwell migration and invasion assay were applied to estimate proliferation, migration and invasion ability of cells. \u0000 \u0000 \u0000Results \u0000The expression of KIF3A protein in the KIF3A-shRNA group cells was significantly silenced compared with those in the Scr-shRNA group cells. The expression of KIF3A in the KIF3A-pEX group cells was increased compared with those in the Vector group cells. The colony numbers in the KIF3A-shRNA group were significantly lower than those in Scr-shRNA group (174.8±46.26 vs. 293.2±20.93, P<0.01). The colony numbers in the KIF3A-pEX group were significantly higher than those in Vector group cells (292.00±75.59 vs. 151.40±68.58, P<0.05). The result of the transwell migrated assay showed that the numbers of migrated cells in the KIF3A-shRNA group were significantly lower than those in Scr-shRNA group (47.60±5.77 vs. 161.40±20.16, P<0.01) and the numbers of migrated cells in the KIF3A-pEX group were significantly higher than those in Vector group (262.00±23.35 vs. 155.00±29.15, P<0.01). It was confirmed via the transwell invasion assay results that the cell’s invasive ability of KIF3A-shRNA group was progressively suppressed as compared with the Scr-shRNA group (161.40±16.16 vs. 281.00±19.77, P<0.01) and the cell’s invasive ability of KIF3A-pEX group was progressively promoted as compared with the Vector group (214.00±34.54 vs. 125.40±19.94, P<0.01). \u0000 \u0000 \u0000Conclusion \u0000Down-regulation of KIF3A in TNBC cell can inhibit the cell proliferation, migration and invasion. Overexpression of KIF3A in TNBC cell can promote the cell proliferation, migration and invasion. KIF3A might hold potential as a therapeutic drug target for human TNBC. \u0000 \u0000 \u0000Key words: \u0000KIF3A; Short hairpin RNA; Triple negative breast cancer; Proliferation; Migration; Invasion","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"36 1","pages":"2173-2175"},"PeriodicalIF":0.0,"publicationDate":"2019-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45790527","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 : 2019-12-08DOI: 10.3760/CMA.J.ISSN.1001-9030.2019.12.054
M. Cui, Q. Liao
Sialylation is one type of glycosylation that adds sialic acid residues to the tip of glycans in glycoprotein or glycolipid on cell membrane and participates in many critical cellular processes via cell-cell contact. The level of sialylation is usually elevated during carcinogenesis. Increased sialic acid could interact with Siglecs on the surface of immune cells, and thus induce immunosuppressive tumor microenvironment and tumor immune escape. It is believed that sialic acid-Siglecs can be served as novel immune checkpoints and bring hope to the development of immunotherapy in the future. Key words: Sialic acid; Cancer; Immune escape; Siglec
{"title":"Hypersialylation promotes tumor immune escape","authors":"M. Cui, Q. Liao","doi":"10.3760/CMA.J.ISSN.1001-9030.2019.12.054","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2019.12.054","url":null,"abstract":"Sialylation is one type of glycosylation that adds sialic acid residues to the tip of glycans in glycoprotein or glycolipid on cell membrane and participates in many critical cellular processes via cell-cell contact. The level of sialylation is usually elevated during carcinogenesis. Increased sialic acid could interact with Siglecs on the surface of immune cells, and thus induce immunosuppressive tumor microenvironment and tumor immune escape. It is believed that sialic acid-Siglecs can be served as novel immune checkpoints and bring hope to the development of immunotherapy in the future. \u0000 \u0000 \u0000Key words: \u0000Sialic acid; Cancer; Immune escape; Siglec","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"36 1","pages":"2295-2298"},"PeriodicalIF":0.0,"publicationDate":"2019-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45339007","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 : 2019-12-08DOI: 10.3760/CMA.J.ISSN.1001-9030.2019.12.044
L. Pan, Xiaozhen Peng, F. Qiang, Liu Chuanjiang, Q. Tao, Z. Hongwei
Objective To investigate the expression of chromobox protein homolog 3 (CBX3) and p53 protein in hepatocellular carcinoma and their correlation. Methods Sixty patients with liver cancer and their corresponding adjacent tissues were selected. Immunofluorescence and Western blotting were used to detect the expression of CBX3 and p53 protein in hepatocarcinoma tissues and adjacent tissues, and to analyze their correlation with tumor size, TNM stage, tumor differentiation, vascular thrombosis and lymph node metastasis. Sex. The χ2 test of the paired data analyzed the correlation between the two proteins. Results The positive expression rates of CBX3 protein and p53 protein in liver cancer tissues were 76.7% and 71.7%, respectively. CBX3 protein expression and tumor size (χ2=5.293, P<0.05), vascular tumor thrombus (χ2=5.671, P<0.05), lymph node metastasis (χ2=4.543, P<0.05), TNM staging (χ2=6.229, P<0.05) and The degree of tumor differentiation (χ2=10.221, P<0.01) was significantly correlated. p53 protein expression and tumor size (χ2=5.844, P<0.05), vascular tumor thrombus (χ2=4.966, P<0.05), lymph node metastasis (χ2=6.570, P<0.05), TNM staging (χ2=5.629, P<0.05), The degree of tumor differentiation (χ2=13.611, P<0.01) was significantly correlated. The expression levels of CBX3 and p53 protein were 10.09-fold and 7.35-fold, respectively, and they were positively correlated (r=0.359, P<0.05). Conclusion The expression of CBX3 and p53 protein is up-regulated in hepatocarcinoma tissues, which is significantly correlated with tumor size, TNM stage, tumor tissue differentiation, vascular thrombosis and lymph node metastasis. CBX3 protein was positively correlated with p53 protein positive expression. Key words: Chromobox protein homolog 3; P53 protein; Liver cancer
{"title":"Expression of chromobox protein homolog 3 and p53 proteins in hepatocellular carcinoma and their correlation with pathological features","authors":"L. Pan, Xiaozhen Peng, F. Qiang, Liu Chuanjiang, Q. Tao, Z. Hongwei","doi":"10.3760/CMA.J.ISSN.1001-9030.2019.12.044","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2019.12.044","url":null,"abstract":"Objective \u0000To investigate the expression of chromobox protein homolog 3 (CBX3) and p53 protein in hepatocellular carcinoma and their correlation. \u0000 \u0000 \u0000Methods \u0000Sixty patients with liver cancer and their corresponding adjacent tissues were selected. Immunofluorescence and Western blotting were used to detect the expression of CBX3 and p53 protein in hepatocarcinoma tissues and adjacent tissues, and to analyze their correlation with tumor size, TNM stage, tumor differentiation, vascular thrombosis and lymph node metastasis. Sex. The χ2 test of the paired data analyzed the correlation between the two proteins. \u0000 \u0000 \u0000Results \u0000The positive expression rates of CBX3 protein and p53 protein in liver cancer tissues were 76.7% and 71.7%, respectively. CBX3 protein expression and tumor size (χ2=5.293, P<0.05), vascular tumor thrombus (χ2=5.671, P<0.05), lymph node metastasis (χ2=4.543, P<0.05), TNM staging (χ2=6.229, P<0.05) and The degree of tumor differentiation (χ2=10.221, P<0.01) was significantly correlated. p53 protein expression and tumor size (χ2=5.844, P<0.05), vascular tumor thrombus (χ2=4.966, P<0.05), lymph node metastasis (χ2=6.570, P<0.05), TNM staging (χ2=5.629, P<0.05), The degree of tumor differentiation (χ2=13.611, P<0.01) was significantly correlated. The expression levels of CBX3 and p53 protein were 10.09-fold and 7.35-fold, respectively, and they were positively correlated (r=0.359, P<0.05). \u0000 \u0000 \u0000Conclusion \u0000The expression of CBX3 and p53 protein is up-regulated in hepatocarcinoma tissues, which is significantly correlated with tumor size, TNM stage, tumor tissue differentiation, vascular thrombosis and lymph node metastasis. CBX3 protein was positively correlated with p53 protein positive expression. \u0000 \u0000 \u0000Key words: \u0000Chromobox protein homolog 3; P53 protein; Liver cancer","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"36 1","pages":"2269-2271"},"PeriodicalIF":0.0,"publicationDate":"2019-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42155947","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 : 2019-12-08DOI: 10.3760/CMA.J.ISSN.1001-9030.2019.12.059
Yinglong Huang, Yi-gang Zuo, Jiansong Wang
Almost all tumors have varying degrees of metabolic changes during the tumorigenesis and development, which are collectively referred to as metabolic reprogramming. Metabolic reprogramming leads to a large difference in the metabolic patterns of glucose, glutamine, fatty acids and other substances in tumor cells, and is also considered to be an important biomarker of cancer. Many studies have confirmed that metabolic reprogramming provides sufficient energy and material basis for the growth of tumor cells, and has a positive impact on the biological behavior of tumor cells. It also has metabolic reprogramming in the occurrence and development of bladder cancer, which plays an important role in maintaining the growth of tumor cells and enhancing the chemoresistance of bladder cancer. Therefore, to explore the correlation between metabolic reprogramming and bladder cancer and its potential mechanisms, to explore specific drug targets and effective interventions, may provide a groundbreaking idea for the prevention and treatment of bladder cancer. Key words: Metabolic reprogramming; Glycolysis; Bladder cancer; Targeted therapy
{"title":"Metabolic reprogramming of tumors and its research progress in bladder cancer","authors":"Yinglong Huang, Yi-gang Zuo, Jiansong Wang","doi":"10.3760/CMA.J.ISSN.1001-9030.2019.12.059","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2019.12.059","url":null,"abstract":"Almost all tumors have varying degrees of metabolic changes during the tumorigenesis and development, which are collectively referred to as metabolic reprogramming. Metabolic reprogramming leads to a large difference in the metabolic patterns of glucose, glutamine, fatty acids and other substances in tumor cells, and is also considered to be an important biomarker of cancer. Many studies have confirmed that metabolic reprogramming provides sufficient energy and material basis for the growth of tumor cells, and has a positive impact on the biological behavior of tumor cells. It also has metabolic reprogramming in the occurrence and development of bladder cancer, which plays an important role in maintaining the growth of tumor cells and enhancing the chemoresistance of bladder cancer. Therefore, to explore the correlation between metabolic reprogramming and bladder cancer and its potential mechanisms, to explore specific drug targets and effective interventions, may provide a groundbreaking idea for the prevention and treatment of bladder cancer. \u0000 \u0000 \u0000Key words: \u0000Metabolic reprogramming; Glycolysis; Bladder cancer; Targeted therapy","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"36 1","pages":"2312-2316"},"PeriodicalIF":0.0,"publicationDate":"2019-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49238513","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 : 2019-12-08DOI: 10.3760/CMA.J.ISSN.1001-9030.2019.12.053
He De, Liu Zhijian, Ma Guangnian, E. Hu, Xu Yumin, Xiong Longhui
{"title":"Analytical application of next-generation sequencing technology for detection of gene mutations in pancreatic cancer","authors":"He De, Liu Zhijian, Ma Guangnian, E. Hu, Xu Yumin, Xiong Longhui","doi":"10.3760/CMA.J.ISSN.1001-9030.2019.12.053","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2019.12.053","url":null,"abstract":"","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"36 1","pages":"2294-2294"},"PeriodicalIF":0.0,"publicationDate":"2019-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48986448","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 : 2019-12-08DOI: 10.3760/CMA.J.ISSN.1001-9030.2019.12.002
Xue-ru Zhu
Prostate cancer is one of the common malignant tumors in Chinese men. Most patients are diagnosed with prostate cancer at an advanced stage, and many patients fail to take the best treatment opportunity. The majority of prostate cancer patients progress to castration-resistant prostate cancer after castration, and their alternative treatment options are limited. Immunotherapy has made many breakthroughs in cancer research, and immunotherapy has been proven to bring survival benefits to patients with cancer. However, different types of immunotherapy regimens benefit differently for prostate cancer patients. This article will describe the therapeutic effects of immunotherapy in prostate cancer and its basis research. Key words: Prostate cancer; Immunotherapy
{"title":"Current strategies and prospects of basic research on prostate cancer immunotherapy","authors":"Xue-ru Zhu","doi":"10.3760/CMA.J.ISSN.1001-9030.2019.12.002","DOIUrl":"https://doi.org/10.3760/CMA.J.ISSN.1001-9030.2019.12.002","url":null,"abstract":"Prostate cancer is one of the common malignant tumors in Chinese men. Most patients are diagnosed with prostate cancer at an advanced stage, and many patients fail to take the best treatment opportunity. The majority of prostate cancer patients progress to castration-resistant prostate cancer after castration, and their alternative treatment options are limited. Immunotherapy has made many breakthroughs in cancer research, and immunotherapy has been proven to bring survival benefits to patients with cancer. However, different types of immunotherapy regimens benefit differently for prostate cancer patients. This article will describe the therapeutic effects of immunotherapy in prostate cancer and its basis research. \u0000 \u0000 \u0000Key words: \u0000Prostate cancer; Immunotherapy","PeriodicalId":10065,"journal":{"name":"中华实验外科杂志","volume":"36 1","pages":"2130-2136"},"PeriodicalIF":0.0,"publicationDate":"2019-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41903415","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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