Abstract:Objective: To study the effects of CLIC1 on the proliferation, invasion and MAPK/ERK pathway of gastric cancer cells induced by cobalt chloride, so as to provide certain ideas for the treatment of diseases. Methods: After cultured gastric cancer cells SGC-7901 in vitro, they were divided into 4 groups, the normal group (group control) and the cobalt chloride treatment group (150um CoCl2 treatment); in the negative transfection group (group si-NC, CoCl2 was treated with 48h and transfected with NC siRNA); CLIC1 interference group (group si-CLIC1, CoCl2 after treatment continued to cultivate 48h, transfected CLIC1siRNA). The cell supernatants were collected, the viability of SGC-7901 cells was detected by MTT; colony formation assay was used to detect colony formation; the scratch test was used to detect the cell transfer ability; transwell cell was used to detect cell migration and invasion; Western blot (WB) was used to detect the expression of MAPK/ERK pathway related proteins. Results: Compared with control group, the inhibition rate, metastasis inhibition rate and E-cadherin protein expression in CoCl2 group and si-NC group increased, the number of colonies, migration and invasion decreased, while the expression of p-ERK1/2, MMP-9 and N-cadherin protein decreased (P<0.05). After inhibiting CLIC1 expression, the inhibition rate, metastasis inhibition rate and E-cadherin protein expression increased further, and the number, migration and invasion of colonies increased. The number and expression of p-ERK1/2, MMP-9 and N-cadherin protein were further decreased (P<0.05). Conclusion: CoCl2 treatment can inhibit the proliferation and invasion of gastric cancer cells, and the inhibition of CLIC1 expression can further inhibit the proliferation and invasion of gastric cancer cells in coordination with CoCl2, which may be related to the inhibition of MAPK/ERK pathway.
王志强, 孙鹏, 高淳, 徐铭, 张云鹏, 程大庆, 王珏. CLIC1对氯化钴诱导的胃癌细胞增殖侵袭及MAPK/ERK通路的影响[J]. 河北医学, 2019, 25(1): 99-103.
WANG Zhiqiang, SUN Peng, GAO Chun, et al. Effects of CLIC1 on Proliferation, Invasion and MAPK/ERK Pathway of Cobalt Chloride-induced Gastric Cancer Cells. HeBei Med, 2019, 25(1): 99-103.
[1] 左婷婷,郑荣寿,曾红梅,等.中国胃癌流行病学现状[J].中国肿瘤临床,2017,44(1):52~58. [2] 伍友兴,桂若虎,郑新平,等.水飞蓟宾抑制缺氧状态下胃癌细胞mTOR磷酸化及HIF-1α表达[J].中国肿瘤生物治疗杂志,2016,23(1):52~56. [3] Ding Q, Li M, Wu X, et al. CLIC1 overexpression is associated with poor prognosis in gallbladder cancer[J]. Tumour Biology the Journal of the International Society for Oncodevelopmental Biology & Medicine, 2015, 36(1):193~198. [4] Zhao W, Mingshu L U, Zhang Q. Chloride intracellular channel 1 regulates migration and invasion in gastric cancer by triggering the ROS-mediated p38 MAPK signaling pathway:[J]. moLecular Medicine Reports, 2016, 12(6):8041~8047. [5] Lu J, Dong Q, Zhang B, et al. Chloride intracellular channel 1(CLIC1) is activated and functions as an oncogene in pancreatic cancer[J]. Medical Oncology, 2015, 32(6):616~622. [6] 郭洋, 吴密璐, 赵君慧,等. 肺癌低氧微环境与化疗耐药相关性研究进展[J]. 中国肺癌杂志, 2014,17(3):265~268. [7] 王育蓉,李艳艳,卢仁隆.Sp1在低氧肝癌细胞血管内皮生长因子转录调控中的作用[J].军事医学,2017,41(7):572~575. [8] 徐峥,陈武桂,孙靖,等.低氧抑制乳腺癌细胞中信号素3A表达并调控成骨前体细胞分化[J].肿瘤,2016,36(12):1298~1306. [9] 刘晓玲,包韩乌云,赵华路,等.在CoCl2模拟低氧条件下HIF-1α直接调控过氧化物酶体增殖物激活受体γ2(PPARγ2)的表达[J].基础医学与临床,2015,35(5):585~589. [10] 张宾,李畅,贾雪峰,等.子宫内膜样腺癌中CLIC1蛋白的表达及临床意义[J].临床肿瘤学杂志,2014,19(1):49~51. [11] Ding Q, Li M, Wu X, et al. CLIC1 overexpression is associated with poor prognosis in gallbladder cancer[J]. Tumour Biology the Journal of the International Society for Oncodevelopmental Biology & Medicine, 2015, 36(1):193~198. [12] Li B P, Mao Y T, Wang Z, et al. CLIC1 Promotes the Progression of Gastric Cancer by Regulating the MAPK/AKT Pathways.[J]. Cellular Physiology & Biochemistry, 2018, 46(3):907~924. [13] 王妍,刘云鹏,曲秀娟,等.RANKL通过激活Akt及ERK介导胃癌细胞迁移[J].中国医科大学学报,2013,42(7):591~594. [14] 马营营,黄煜,颜莉莉,等.ERK信号转导通路在CXCL12促进子宫内膜癌细胞增殖和侵袭中的作用[J].中国肿瘤生物治疗杂志,2016,23(2):250~254.