miR-101调控非小细胞肺癌的发病机制

目的探讨miR-101在非小细胞肺癌发生、发展中的作用以及新的分子调控机制。方法将miR-101转染到非小细胞肺癌A549细胞株,比较测量人类非小细胞肺癌组织及癌旁组织的miR-101表达水平。采用生物信息学技术预测miR-101在c-Fos的3′UTR潜在结合靶点,然后采用Western blot法和基因敲除方法检测c-Fos的表达和功能。结果分析miR-101在非小细胞肺癌组织及癌旁组织表达,miR-101在非小细胞肺癌组织中低表达(0.00010±0.00002 vs 0.00021±0.00003,P=0.036),过表达miR-101抑制非小细胞肺癌A549细胞增殖并诱导细胞凋亡。并且在非小细胞肺癌细胞中敲除c-Fos和过表达miR-101有相似的效果。结论 miR-101通过c-Fos靶点调节非小细胞肺癌细胞的生长,因此调控miR-101和c-Fos可以应用于非小细胞肺癌潜在的分子治疗。

The pathogenesis of miR-101 in the regulation of non-small cell lung cancer

Objective To investigate the role of miR-101 in the development and progression of non-small cell lung cancer and its new molecular regulation mechanism.Methods miR-101 was transfected into non-small cell lung cancer A549 cell line,and the expression level of miR-101 in human non-small cell lung cancer tissues and adjacent tissues was compared.The bioinformatics technique was used to predict the potential binding of miR-101 to the 3''UTR of c-Fos,and then the expression and function of c-Fos were detected by Western blot and gene knockout.Results The expression of miR-101 in non-small cell lung cancer tissues and adjacent tissues was analyzed.miR-101 was downregulated in non-small cell lung cancer tissues(0.00010±0.00002 vs 0.00021±0.00003,P=0.036).And overexpression of miR-101 was inhibited.Overexpression of miR-101 inhibited proliferation and induced apoptosis in non-small cell lung cancer A549 cells.And knocking out c-Fos and overexpressing miR-101 in non-small cell lung cancer cells had similar effects.Conclusion miR-101 regulates the growth of non-small cell lung cancer cells through c-Fos target,so the regulation of miR-101 and c-Fos can be applied to the potential molecular therapy of non-small cell lung cancer.