摘要
目的:探讨整合素αvβ6对结肠癌细胞中整合素αvβ5内吞胞吐循环及细胞黏附、迁移能力的影响。方法:采用Western blotting检测不同细胞中整合素αvβ6和αvβ5的表达情况,通过整合素内吞实验、胞吐实验和capture-ELISA实验检测不同细胞中整合素αvβ6和αvβ5的内吞胞吐循环时相,利用细胞黏附实验和细胞迁移实验检测各种细胞在不同基质表面黏附和迁移能力的差异。结果:SW480、SW480 wild-typeβ6和SW480 mock细胞中整合素αv亚基和β5亚基的表达无显著差异(P>0.05),SW480 wild-typeβ6细胞中整合素β6亚基的表达显著高于另外2种细胞(P<0.05);SW480细胞中整合素αvβ5存在内吞胞吐循环,但当向SW480细胞中转染β6亚基后,整合素αvβ6进行内吞胞吐循环的同时,会对整合素αvβ5的内吞和胞吐过程产生抑制作用,差异有统计学意义(P<0.05);3种细胞中整合素αvβ6和αvβ5的内吞胞吐循环的差异,会影响细胞在纤连蛋白(整合素αvβ6配体)和玻连蛋白(整合素αvβ5配体)表面的黏附和迁移能力。结论:整合素αvβ6和αvβ5拥有共同的α亚基,它们在细胞内的内吞胞吐循环存在某种竞争性关系,当二者同时存在时,整合素αvβ6会抑制αvβ5的内吞胞吐循环过程,并由此对细胞在相应基质表面黏附和迁移能力产生影响。
AIM ： To investigate the effects of integrin αvβ6 on the endo - exocytotic cycle of integrin αvβ5 in colon cancer cells. METHODS ： The expression of integrin αvβ6 and αvβ5 in SW480 cells, SW480 wild - type αvβ6 cells and SW480 mock cells was detected by Western blotting. The trafficking of integrin αvβ6 and αvβ5 was examined by endo- cytosis assay, exocytosis assay and capture - ELISA. The adhesive and migration abilities of these 3 cell lines towards fi- bronectin or vitronectin were measured by cell adhesion assay and cell migration assay. RESULTS ： The expression of inte- grin αv and β5 subunits was similar in these 3 cell lines （ P 〉 0.05 ）, while the expression of integrin β6 subunit in SW480 wild - type β6 cells was much higher than that in the other 2 cell lines （ P 〈 0.05 ）. The transfection of integrin β6 subunit into SW480 cells was able to slow down the endocytosis and exocytosis of integrin αvβ5, and subsequently inhibited the cel- lular adhesion and migration abilities towards vitronectin. CONCLUSION： Integrin αvβ6 and αvβ5 share the same αv subunit. In the process of endocytosis and exocytosis, there might be some competitive relationship between these 2 integrin isoforms. Compared with integrin αvβ5, integrin αvβ6 has the priority to get into the trafficking process, and it has subse- quent effects on the adhesion and migration of colon cancer cells.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2012年第12期2154-2159,共6页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助项目(No.30570833
No.30872460)
