中文摘要：

目的：探讨慢病毒介导d6整合素（integrinα6，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1TGA6的表达，显微镜下观察Hd60SM细胞形态的变化，MTS法检测细胞增殖，软琼脂实验检测Hd60SM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）w（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]。Hd60SM-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、G0／G1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）％w（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。

英文摘要：

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. 041, [0.22 ±0. 041, 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 G0/G1 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 ±1.381% vs [18.87±1.471%, [18.85±1.111%, P〈0.05）, and the migration rate （[100.00 ＋0.50]% vs [43.92 ＋0.411%, [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-inde