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作 者:许鹤洋[1] 刁飞宇[1] 曾育杰[1] 张旸[1] 来伟[1] 褚忠华[1]
机构地区:[1]中山大学孙逸仙纪念医院胃肠外科,广州510288
出 处:《中华实验外科杂志》2013年第8期1666-1667,共2页Chinese Journal of Experimental Surgery
基 金:广东省自然科学基金自由申请项目(10151008901000071);广东省自然科学基金资助项目(S2012010009161);广东省社会发展计划基金资助项目(201211050600014)
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Westernblot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Westernblot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。Objective To investigate the interaction between colon cancer cells and tumor associ- ated cells (M2) , and it' s influence to tumor cells' function. Methods LoVo cells [ transfeeted with pro- tein tyrosine phosphatase 3 (PRL-3) ] and M2 cells were coeultured, Western blot were used to examine Ca2+ -activated K+ channels (KCNN4) expression of M2 cells. And the invasion of LoVo cells also he de- tected. Results Used by Western blotting it is found out that KCNN4 of M2 cells is improved after eoeul- tured with PRL-3 LoVo cells. Besides, eocuhure 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.
关 键 词:蛋白酪氨酸磷酸酶-3 肿瘤性巨噬细胞 钙离子依赖性钾离子通道
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