CAJ | 학술논문

目的：探讨microRNA-130a（miR-130a）在非小细胞肺癌中的表达情况，并对其功能和分子机制进行研究。方法：收集50例非小细胞肺癌肿瘤组织和相对应的正常肺组织，采用 RT-PCR方法检测miR-130a的相对表达量，并分析其与临床病理资料的相关性。采用体外转染法将miR-130a抑制剂瞬时转染到A549细胞后，应用real-time PCR检测A549细胞中miR-130a的表达情况。CCK8实验检测细胞转染后的增殖变化。Western blot检测转染后细胞中Smad4的表达变化。结果：肺癌组织中miR-130a的表达水平明显高于正常肺组织（ P＜0.05）；miR-130a的表达水平与肿瘤大小、淋巴结转移和临床分期明显相关（ P＜0.05）。与对照组比较，A549细胞转染miR-130a抑制剂后miR-130a表达水平明显下调，细胞增殖率明显下降，差异具有统计学意义（P＜0.05）；转染miR-130a抑制剂后，肺癌细胞中Smad4的表达水平明显上调。结论：miR-130a在NSCLC组织中表达上调，可能部分通过下调Smad4的表达来促进肺癌细胞的增殖和转移。
목적：탐토microRNA-130a（miR-130a）재비소세포폐암중적표체정황，병대기공능화분자궤제진행연구。방법：수집50례비소세포폐암종류조직화상대응적정상폐조직，채용 RT-PCR방법검측miR-130a적상대표체량，병분석기여림상병리자료적상관성。채용체외전염법장miR-130a억제제순시전염도A549세포후，응용real-time PCR검측A549세포중miR-130a적표체정황。CCK8실험검측세포전염후적증식변화。Western blot검측전염후세포중Smad4적표체변화。결과：폐암조직중miR-130a적표체수평명현고우정상폐조직（ P＜0.05）；miR-130a적표체수평여종류대소、림파결전이화림상분기명현상관（ P＜0.05）。여대조조비교，A549세포전염miR-130a억제제후miR-130a표체수평명현하조，세포증식솔명현하강，차이구유통계학의의（P＜0.05）；전염miR-130a억제제후，폐암세포중Smad4적표체수평명현상조。결론：miR-130a재NSCLC조직중표체상조，가능부분통과하조Smad4적표체래촉진폐암세포적증식화전이。
Objective:To investigate the exPression of miR-130a in Patients with non-small cell lung cancer (NSCLC)and to analyze the function and mechanism of miR-130a. Methods:The exPression levels of miR-130a in 50 tumor tissues and Paired normal tissues of NSCLC were detected by using RT-PCR. The relationshiP between the level of miR-130a and the Pathological characteristics was analyzed. miR-130a in vitro was transiently trans-ferred into A549 cells. The exPression level of miR-130a in A549 cells was detected by RT-PCR. Cell viability was analyzed by CCK8 assay. ExPression of Smad4 Protein was detected by Western blot. Results:The exPression level of miR-130a was uP-regulated in tumor tissues as comPared with normal lung tissues(P<0. 05). The exPression of miR-130a was associated with tumor size,lymPhatic metastasis,and TNM stages(P<0. 05). miR-130a in anti-miR-130a-transfected A549 cells was significantly decreased comPared with the control grouP(P<0. 05). The Proliferation of anti-miR-130a-transfected A549 cells was inhibited significantly. The exPression level of Smad4 was markedly uP-regulated after transfection(P<0. 05). Conclusion:The exPression of miR-130a was uP-regu-lated in NSCLC,miR-130a might Promote Proliferation and metastasis of lung cancer in Part by down-regulating the exPression of Smad4.