[摘要] 目的：探讨miR-23b/PTEN 分子轴对肺癌A549 细胞放疗敏感性的影响及其作用机制。方法：选用人肺癌细胞系NCI-H1650、NCI-H175、Calu-1、LTEP-A-2、MSTO-211H、A549 及正常肺上皮细胞株BEAS-2B，用qPCR 检测肺癌细胞系中miR-23b 的表达水平。用双荧光素酶报告基因检测miR-23b 和PTEN的靶向关系。用脂质体转染技术将miR-23b mimics、miR-23b inhibitor、pcDNA3.1-PTEN 等不同质粒转染进A549 细胞，用WB检测细胞中PTEN的表达水平，用CCK-8、Transwell 和Annexin VFITC/PI 染色流式细胞术分别检测miR-23b/PTEN分子轴对60Co γ-射线处理的A549 细胞增殖、侵袭和凋亡的影响。结果：miR-23b 在肺癌细胞系中高表达（P<0.05 或P<0.01），尤其在A549 细胞中表达水平最高（P<0.01）。敲降miR-23b 可逆转3 Gy60Co γ-射线对A549 细胞增殖和侵袭的抑制作用，并诱导细胞凋亡（P<0.05 或P<0.01）。双荧光素酶报告基因结果显示，miR-23b 可靶向负调控PTEN（P<0.05）。敲降miR-23b 能上调PTEN 的表达水平，进而上调3 Gy 60Co γ-射线对A549 细胞凋亡的促进作用及抑制A549 细胞增殖和侵袭（P<0.05 或P<0.01）。结论：敲降miR-23b 可以增强肺癌A549 细胞的放疗敏感性，其机制是60Co γ-射线通过下调miR-23b 对PTEN表达的抑制，进而降低A549 细胞增殖、侵袭能力并诱导细胞凋亡。

[Abstract] Objective: To investigate the effect of miR-23b/PTEN molecular axis on radio-sensitivity of lung cancer A549 cells and its mechanism. Methods: Lung cancer cell lines NCI-H1650, NCI-H175, Calu-1, LT-P-A-2, MSTO-211H, A549 and human normal lung epithelial cell line BEAS-2B were selected. The expression level of miR-23b in lung cancer cell lines was detected by qPCR. Dual-luciferase reporter gene assay was used to verify the relationship between miR-23b and PTEN. Plasmids miR-23b mimics, miR-23b inhibitor and pcDNA3.1-PTEN were transfected into A549 cells by lipofection; PTEN expression levels in cells was detected by WB. CCK-8,Transwell and Annexin V-FITC/PI staining flow cytometry were used to detect the effect of miR-23b/PTEN axis on proliferation, invasion and apoptosis of A549 cells treated with 60Co γ-ray. Results: miR-23b was upregulated in lung cancer cell lines with the highest expression in A549 cells (P<0.05 or P<0.01). Knockdown of miR-23b reversed the inhibitory effect of 3 Gy 60Co γ-rays on proliferation and invasion of A549 cells, and induced apoptosis (P<0.05 or P<0.01). Dual-luciferase reporter gene assay results confirmed that miR-23b could negatively regulate PTEN (P<0.05). Furthermore, knockdown of miR-23b up-regulated PTEN expression level, and furhter enhanced the inhibitory effect of 3 Gy 60Co γ-ray on the proliferation and invasion of A549 cells as well as induced apoptosis of A549 cells (P<0.05 or P<0.01). Conclusion: Knockdown of miR-23b can enhance the radio-sensitivity of A549 cells, the mechanism of which is that 60Co γ-ray down-regulates the inhibitory effect of miR-23b on PTEN, thereby inhibiting the proliferation, invasion and inducing apoptosis of A549 cells.