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目的探讨内源性过表达人整合素连接激酶(integrin-linked kinase,ILK)及外源性脂多糖(lipopolysaccharide,LPS)对肺癌A549细胞分泌VEGF、TGF-β、IL-6的相关性。方法分别设置空白对照组、过表达ILK组、LPS诱导组、LPS诱导过表达ILK组,通过ELISA双抗夹心法,分别检测各组细胞分泌VEGF、TGF-β、IL-6的水平;应用RT-PCR法检测各组细胞磷脂酰肌醇3-激酶(phosphatidylinositol 3-kinase,PI3K)p85α的相对转录水平。结果过表达ILK组、空白细胞的培养上清液和细胞裂解液相比较,各因子水平无显著差异(P>0.05);与对照组相比较,过表达ILK组和LPS诱导组细胞所分泌的VEGF、TGF-β、IL-6因子的水平均显著增高,差异具有统计学意义(P<0.05),且LPS诱导的ILK过表达组的各因子升高更为显著(P<0.05);LPS诱导组细胞的PI3Kp85α的相对转录水平显著高于过表达ILK组和空白对照组(P<0.05)。结论内源性过表达ILK基因和外源性LPS诱导均可促进A549细胞产生免疫逃逸相关因子,LPS促瘤效应机制可能与ILK相关,LPS可能通过PI3K信号分子促进了ILK的生物学效应。
Objective To investigate the correlation between endogenous over-expression of human integrin-linked kinase (ILK) and exogenous lipopolysaccharide (LPS) on the secretion of VEGF, TGF-β and IL-6 in A549 lung cancer cells. Methods The control group, ILK group, LPS-induced group and LPS-induced ILK group were established. The levels of VEGF, TGF-β and IL-6 secreted by each group were detected by ELISA. The relative transcription level of phosphatidylinositol 3-kinase (PI3K) p85α in each group was detected by PCR. Results Compared with the control group, the levels of ILK and LPS-induced cells in supernatants of ILK group and blank cells were not significantly different (P> 0.05) The levels of VEGF, TGF-β and IL-6 were significantly increased (P <0.05), and the increase of LPS-induced ILK over-expression was more significant (P <0.05). The levels of LPS The relative transcription level of PI3Kp85α in induced cells was significantly higher than that in overexpression ILK group and blank control group (P <0.05). Conclusions Both endogenous overexpression of ILK gene and exogenous LPS can promote immune escape-related factors in A549 cells. The mechanism of LPS promoting tumorigenesis may be related to ILK. LPS may promote the biological effects of ILK through PI3K signaling molecules.