Hedgehog信号通路在胃癌细胞中活化并通过GLI1促进MKN28细胞增殖

目的研究Hedgehog：（HH）信号通路在胃癌细胞中的活化形式及其转录因子GLI1对胃癌细胞增殖和体外成瘤能力的影响。方法通过反转录PCR分析HH通路相关组成分子在7株细胞系中的表达情况．化学合成针对HH信号通路转录因子GLI1的siRNA并转染胃癌MKN28细胞。通过CCK8法和体外克隆形成实验．观察GLII siRNA转染胃癌MKN28细胞后的细胞增殖能力和克隆形成能力的变化。结果在不同胃癌细胞株中．HH信号通路各相关基因的表达情况存在差异，SHH在6株胃癌细胞系中均表达上调．PTCH在KATOⅢ细胞系、SUFU在MKN28和KATOⅢ表达下调。转染GLI1 siRNA后，MKN28细胞中GLI1 mRNA表达受到明显抑制；经GLI1 siRNA作用的MKN28细胞生长明显缓于阴性对照和未处理组（P=0．014），克隆形成数目及体外克隆形成能力降低（P〈0．001）。结论HH信号通路在胃癌细胞系中被普遍激活，HH信号通路活化后可通过转录因子GLI1促进MKN28细胞增殖．

Hedgehog signaling pathway activates in gastric carcinoma and promotes the proliferation through GLI1 in MKN28 cell

Objective To investigate the effect of Hedgehog(HH) pathway on proliferation and in vitro tumorigenicity of gastric cancer cell lines. Methods The expression of SHH, PTCH, SMO, SUFU and GLI1 in seven cell lines were tested by RT-PCR. siRNA targeting GLI1 mRNA was transfected into MKN28 cells. Cell proliferation and in vitro tumorigenicity were examined by CCK8 and soft agar colony formation test. Results SHH in six gastric cancer cell lines was up-regulated. Expression of PTCH in KATO Ⅲ cell lines and expression of SUFU in MKN28 and KATO Ⅲ were reduced. GLI1 siRNA significantly inhibited the expression of GLI1 in MKN28 cell line. Growth rate and colony formation rate of MKN28 cells treated with GLI1 siRNA were significantly lower than those of control cells (all P<0.001 ). Conclusions HH signaling pathway is widely activated in gastric cancer cell lines. The activation of HH signaling pathway promotes the growth of MKN28 cells.