CLIC1对氯化钴诱导的胃癌细胞增殖侵袭及MAPK/ERK通路的影响

doi:10.3969/j.issn.1006-6233.2019.01.025

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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.

Key words： Gastric cancer Cobalt chloride CLIC1

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http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2019.01.025 OR http://www.hbyxzzs.cn/EN/Y2019/V25/I1/99

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