目的： 探讨慢病毒介导α6整合素（integrin α6, ITGA6）shRNA对人非小细胞肺癌（non-small cell lung cancer，NSCLC）H460SM细胞生长和侵袭的影响。 方法： 实时定量PCR和Western blotting检测ITGA6在9种NSCLC细胞中的表达。慢病毒介导ITGA6shRNA感染H460SM细胞后，实时定量PCR和Wesern blotting检测H460SM中ITGA6的表达，显微镜下观察H460SM细胞形态的变化，MTS法检测细胞增殖，软琼脂实验检测H460SM细胞锚定非依赖性生长，流式细胞术检测细胞凋亡和细胞周期，迁移和侵袭实验检测H460SM细胞体外迁移和侵袭能力。 结果：ITGA6在7种人NSCLC细胞中均有表达，H460SM细胞中ITGA6表达水平明显高于亲本H460细胞\[ (8.75±0.09) vs (5.78±0.26)，P<0.01 \]。慢病毒介导ITGA6shRNA稳定感染H460SM细胞后的H460SM-75、H460SM-76细胞中，ITGA6表达水平明显低于阴性对照组H460SM-NS细胞\[(0.11±0.04)、(0.22±0.04) vs (1.00±0.01)，P<0.01\]。H460SM-75、H460SM-76细胞增殖活性与H460SM-NS细胞无差异（P>0.05），且凋亡率、细胞增殖指数、G0/G1期细胞的比例也无差异（P>0.05）。H460SM-75、H460SM-76细胞的克隆形成率明显低于H460SM-NS细胞 \[(18.87±1.47)%、(18.85±1.11)% vs (20.81±138)%，P<005\]，迁移率\[(43.92±041)%、(24.10±0.33)% vs (100.00±0.50)% ，P<0.01 \]和侵袭率\[ (7.04±296)%、(4.68±0.27)% vs (100.00±674)%， P<0.01\]也明显低于H460SM-NS细胞。 结论： 抑制ITGA6的表达可以抑制NSCLC细胞锚定非依赖性生长、迁移和侵袭，但不影响NSCLC细胞增殖和凋亡。

Objective: To investigate the effect of lentivirus-mediated integrin α6 (ITGA6) shRNA on growth and invasion of human non-small cell lung cancer (NSCLC) H460SM cells. Methods: The expression levels of ITGA6 in 9 human NSCLC cell lines were evaluated by quantitative-PCR (Q-PCR) and Western blotting. Lentiviral ITGA6 shRNA were transfected into H460SM cells and ITGA6expression was detected by Q-PCR and Western blotting; the cellular morphology change was observed under a microscope; cell proliferation was detected by MTS assay; anchorage-independent growth was determined by colony formation assay in soft agar; apoptosis and cell cycle were analyzed by flow cytometry; and cell invasion and migration were determined by invasion and migration assay. Results: ITGA6 was expressed in 7 NSCLC cell lines. A significantly higher level of ITGA6 expression was seen in H460SM cells compared with the parental H460 cells (\[8.75±0.09\] vs \[5.78±0.26\], P<0.01). After H460SM cells were stably transfected with lentiviral ITGA6 shRNA (H460SM-75, H460SM-76 cells), a significant down-regulation of ITGA6 expression was observed in H460SM-75 and H460SM-76 cells compared with negative control H460SM-NS cells (\[1.00±0.01\] vs \[0.11±0.04\], \[0.22±004\], P<0.01). The cell viability of H460SM-75 and H460SM-76 cells had no difference with H460SM-NS cells (P>0.05), as well as the apoptotic rate, cell proliferative index and proportion of G0/G1 phase cells as compared with the negative control (P>0.05). The colony formation rate of H460SM-75 and H460SM-76 cells was significantly decreased as compared with H460SM-NS cells (\[20.81±1.38\]% vs \[18.87±1.47\]%, \[18.85±1.11\]%, P<0.05), and the migration rate (\[100.00±0.50\]% vs \[43.92±0.41\]%, \[24.10±0.33\]%, P<0.01) and invasion rate (\[100.00±6.74\]% vs \[7.04±2.96\]%, \[4.68±0.27\]%, P<0.01) were also significantly decreased. Conclusion: Knockdown of ITGA6 expression can inhibit anchorage-independent cell growth, migration and invasion of NSCLC cells, but have no effect on cell proliferation and apoptosis.

国家自然科学基金资助项目（No. 81060177）；云南省应用基础研究基金资助项目（No. 2009CD181）；中国人事部留学人员科技活动项目择优资助启动基金资助项目（No.人社厅\[2010\]412号）；云南省卫生科技基金资助项目（No. 2009NS079）