BOP1对胃癌BGC823细胞迁移和侵袭的影响
|
摘要
目的探讨增殖阻断蛋白1(BOP1)在人胃癌组织和癌旁正常胃组织中的表达情况及其对胃癌细胞迁移和侵袭的影响。方法 Real-time PCR和Western blot检测胃癌组织、正常胃组织、胃黏膜正常上皮细胞GES1和胃癌细胞BGC823中BOP1 mRNA和蛋白的表达水平;通过siRNA沉默BGC823细胞中的BOP1基因,然后进行划痕实验以及Transwell小室迁移和侵袭实验,以检测沉默该基因对胃癌细胞迁移和侵袭的影响。结果 BOP1 mRNA和蛋白在胃癌组织和胃癌细胞中的表达高于正常胃组织和胃黏膜正常上皮细胞;沉默BOP1基因后BGC823细胞BOP1的表达水平明显下降;与空白对照组和阴性对照组相比,BOP1沉默组胃癌细胞迁移和侵袭的能力明显下降。结论 BOP1在胃癌组织和胃癌细胞中高表达,并可促进胃癌细胞的迁移和侵袭。
Objective To investigate the expression of block of proliferation 1(BOP1) in human gastric cancer tissues and adjacent normal gastric tissues and its influence on the migration and invasion of gastric cancer cells.Methods Real-time PCR and Western blot were used to detect the expression level of BOP1 mRNA and protein in gastric cancer tissue, normal stomach tissue, normal gastric epithelial cells GES1 and gastric cancer cells BGC823. The BOP1 gene in BGC823 cells was silenced by siRNA, followed by scratch experiments and Transwell chamber migration and invasion experiments to detect the effect of silencing the gene on the migration and invasion of gastric cancer cells.Results The expression of BOP1 mRNA and protein in gastric cancer tissues and gastric cancer cells was higher than that in normal gastric tissues and normal gastric mucosa epithelial cells. The expression of BOP1 in BGC823 cells was significantly decreased after BOP1 gene was silenced. The ability of gastric cancer cells to migrate and invade in BOP1 silencing group was significantly decreased.Conclusion BOP1 is highly expressed in gastric cancer tissues and gastric cancer cells and can promote the migration and invasion of gastric cancer cells.
Objective To investigate the expression of block of proliferation 1(BOP1) in human gastric cancer tissues and adjacent normal gastric tissues and its influence on the migration and invasion of gastric cancer cells.Methods Real-time PCR and Western blot were used to detect the expression level of BOP1 mRNA and protein in gastric cancer tissue, normal stomach tissue, normal gastric epithelial cells GES1 and gastric cancer cells BGC823. The BOP1 gene in BGC823 cells was silenced by siRNA, followed by scratch experiments and Transwell chamber migration and invasion experiments to detect the effect of silencing the gene on the migration and invasion of gastric cancer cells.Results The expression of BOP1 mRNA and protein in gastric cancer tissues and gastric cancer cells was higher than that in normal gastric tissues and normal gastric mucosa epithelial cells. The expression of BOP1 in BGC823 cells was significantly decreased after BOP1 gene was silenced. The ability of gastric cancer cells to migrate and invade in BOP1 silencing group was significantly decreased.Conclusion BOP1 is highly expressed in gastric cancer tissues and gastric cancer cells and can promote the migration and invasion of gastric cancer cells.
引文
[1] Chen W, Zheng R, Zhang S, et al. Cancer incidence and mortality in China in 2013:an analysis based on urbanization level[J].Chinese J Cancer Res,2017, 29(1):1-10.
[2] Ghosn M, Tabchi S, Kourie H R, et al. Metastatic gastric cancer treatment: Second line and beyond[J]. World J Gastroenterol, 2016, 22(11):3069-77.
[3] Pestov D G, Grzeszkiewicz T M, Lau L F. Isolation of growth suppressors from a cDNA expression library[J]. Oncogene, 1998, 17(24):3187-97.
[4] Killian A, Sarafan-Vasseur N, Sesboüé R, et al. Contribution of the BOP1, gene, located on 8q24, to colorectal tumorigenesis[J].Gene Chromosome Canc, 2006, 45(9):874-81.
[5] Qi J, Yong Y, ?zlem A ?, et al. New Wnt/β-catenin target genes promote experimental metastasis and migration of colorectal cancer cells through different signals[J]. Gut, 2016, 65(10):1690-701.
[6] Chung K Y, Cheng I K, Ching A K, et al. Block of proliferation 1(BOP1) plays an oncogenic role in hepatocellular carcinoma by promoting epithelial-to-mesenchymal transition[J]. Hepatology, 2011, 54(1):307-18.
[7] Lee J H, Horak C E, Khanna C, et al. Alterations in Gemin5 expression contribute to alternative mRNA splicing patterns and tumor cell motility[J]. Cancer Research,2008,68(3):639-44.
[8] Catalano V, Labianca R, Beretta G D, et al. Gastric cancer[J]. Crit Rev Oncol Hematol, 2009, 71(2):127-64.
[9] Van Cutsem E, Sagaert X, Topal B,et al. Gastric cancer[J]. Lancet, 2016, 388(10060): 2654-64.
[10] Li M, Zhou Y, Chen P, et al. Genetic variants on chromosome 8q24 and colorectal neoplasia risk: a case-control study in China and a meta-analysis of the published literature[J]. PLoS One, 2011, 6(3): e18251.
[11] Guo Y, Fang J, Liu Y, et al. Association between polymorphism rs6983267 and gastric cancer risk in Chinese population[J]. World J Gastroentero,2011, 17(13):1759-65.
[12] Montanaro L, Trer D, Derenzini M. Nucleolus, ribosomes, and cancer[J].AM J Pathol, 2008, 173(2):301-10.
[13] Karim M E, Tha K K, Othman I, et al. Therapeutic potency of nanoformulations of siRNAs and shRNAs in animal models of cancers[J]. Pharmaceutics, 2018, 10(2): E65.
[14] Natalwala A, Spychal R, Tselepis C. Epithelial-mesenchymal transition mediated tumourigenesis in the gastrointestinal tract[J].World J Gastroentero,2008, 14(24):3792-7.
[15] Wong S, Fang C M, Chuah L H, et al. E-cadherin: its dysregulation in carcinogenesis and clinical implications[J]. Crit Rev Oncol Hematol,2018, 121:11-22.
[2] Ghosn M, Tabchi S, Kourie H R, et al. Metastatic gastric cancer treatment: Second line and beyond[J]. World J Gastroenterol, 2016, 22(11):3069-77.
[3] Pestov D G, Grzeszkiewicz T M, Lau L F. Isolation of growth suppressors from a cDNA expression library[J]. Oncogene, 1998, 17(24):3187-97.
[4] Killian A, Sarafan-Vasseur N, Sesboüé R, et al. Contribution of the BOP1, gene, located on 8q24, to colorectal tumorigenesis[J].Gene Chromosome Canc, 2006, 45(9):874-81.
[5] Qi J, Yong Y, ?zlem A ?, et al. New Wnt/β-catenin target genes promote experimental metastasis and migration of colorectal cancer cells through different signals[J]. Gut, 2016, 65(10):1690-701.
[6] Chung K Y, Cheng I K, Ching A K, et al. Block of proliferation 1(BOP1) plays an oncogenic role in hepatocellular carcinoma by promoting epithelial-to-mesenchymal transition[J]. Hepatology, 2011, 54(1):307-18.
[7] Lee J H, Horak C E, Khanna C, et al. Alterations in Gemin5 expression contribute to alternative mRNA splicing patterns and tumor cell motility[J]. Cancer Research,2008,68(3):639-44.
[8] Catalano V, Labianca R, Beretta G D, et al. Gastric cancer[J]. Crit Rev Oncol Hematol, 2009, 71(2):127-64.
[9] Van Cutsem E, Sagaert X, Topal B,et al. Gastric cancer[J]. Lancet, 2016, 388(10060): 2654-64.
[10] Li M, Zhou Y, Chen P, et al. Genetic variants on chromosome 8q24 and colorectal neoplasia risk: a case-control study in China and a meta-analysis of the published literature[J]. PLoS One, 2011, 6(3): e18251.
[11] Guo Y, Fang J, Liu Y, et al. Association between polymorphism rs6983267 and gastric cancer risk in Chinese population[J]. World J Gastroentero,2011, 17(13):1759-65.
[12] Montanaro L, Trer D, Derenzini M. Nucleolus, ribosomes, and cancer[J].AM J Pathol, 2008, 173(2):301-10.
[13] Karim M E, Tha K K, Othman I, et al. Therapeutic potency of nanoformulations of siRNAs and shRNAs in animal models of cancers[J]. Pharmaceutics, 2018, 10(2): E65.
[14] Natalwala A, Spychal R, Tselepis C. Epithelial-mesenchymal transition mediated tumourigenesis in the gastrointestinal tract[J].World J Gastroentero,2008, 14(24):3792-7.
[15] Wong S, Fang C M, Chuah L H, et al. E-cadherin: its dysregulation in carcinogenesis and clinical implications[J]. Crit Rev Oncol Hematol,2018, 121:11-22.