摘要目的 观察结肠癌肿瘤微环境中肿瘤细胞与巨噬细胞(M2)相互作用及对肿瘤细胞功能学的改变.方法 将转入蛋白酪氨酸磷酸酶-3(PRL-3)的LoVo细胞和M2细胞模拟肿瘤微环境进行共培养,通过Western blot检测M2细胞钙离子依赖性钾离子通道(KCNN4)蛋白表达,并检测LoVo细胞侵袭性的改变.结果 Western blot检测示PRL-3能通过共培养后诱导M2细胞KCNN4蛋白表达升高,而未作共培养的M2细胞KCNN4蛋白表达未升高.此外,经过共培养后LoVo细胞侵袭性升高(3367±135比1442±89,P＜0.05),而在阻断KCNN4蛋白表达后,LoVo细胞侵袭性降低(1388 ±87比2893±163,P＜0.05).结论 PRL-3在结肠癌肿瘤微环境中通过提高KCNN4表达从而增强LoVo细胞的侵袭性.

abstractsObjective To investigate the interaction between colon cancer cells and tumor associated cells (M2),and it' s influence to tumor cells' function.Methods LoVo cells [transfected with protein tyrosine phosphatase 3 (PRL-3)] and M2 cells were cocultured,Western blot were used to examine Ca2 +-activated K + channels (KCNN4) expression of M2 cells.And the invasion of LoVo cells also be detected.Results Used by Western blotting it is found out that KCNN4 of M2 cells is improved after cocultured with PRL-3 LoVo cells.Besides,coculture also improves the invasion of LoVo cells(3367 ± 135 vs.1442 ± 89,P ＜ 0.05).When KCNN4 expression was blocked,the invasion of LoVo cells is reduced (1388 ±-87 vs.2893-± 163,P ＜0.05).Conclusion PRL-3 improves the invasion of LoVo cells through upregulating KCNN4 of M2 cells in the colon cancer microenvironment.