Zhu Changliang, Zhao Yachao, Zhang Zhipei, Ni Yunfeng, Li Xiaofei, Yong Han
Department of Thoracic Surgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.
Department of Thoracic Surgery, The 309th Hospital of the Chinese PLA, Beijing 100091, P.R. China.
Mol Med Rep. 2015 May;11(5):3647-51. doi: 10.3892/mmr.2014.3134. Epub 2014 Dec 24.
MicroRNAs (miRNAs) are short, non‑coding RNAs that are aberrantly expressed in tumors. miRNA‑33a (miR‑33a) is closely associated with cholesterol metabolism and is essential for cellular growth. The aim of the present study was to explore the role of miR‑33a and identify its clinical significance in lung cancer cells. miR‑33a was observed to be overexpressed in the lung cancer cell lines A549 and NCI‑H460. MTT assay results demonstrated that the overexpression of miR‑33a significantly inhibited the proliferation of A549 cells, and similar results were obtained from the colony formation assay. This suggests that transfection of miR‑33a may suppress the growth of lung cancer cells. Overexpression of miR‑33a was also observed to result in marked G1/S phase cell cycle arrest in A549 and NCI‑H460 cell lines using fluorescence‑activated cell sorting analysis. Western blot analysis revealed that overexpression of miR‑33a significantly reduced the expression of β‑catenin in A549 and NCI‑H460 cells, suggesting a direct or indirect regulation of β‑catenin by miR‑33a in lung cancer cells. In conclusion, the current study may provide strategies for the treatment of lung cancer and clarify the mechanism of its progression.
微小RNA（miRNA）是短链非编码RNA，在肿瘤中表达异常。miRNA-33a（miR-33a）与胆固醇代谢密切相关，对细胞生长至关重要。本研究旨在探讨miR-33a在肺癌细胞中的作用并确定其临床意义。观察到miR-33a在肺癌细胞系A549和NCI-H460中过表达。MTT试验结果表明，miR-33a的过表达显著抑制了A549细胞的增殖，集落形成试验也得到了类似结果。这表明转染miR-33a可能抑制肺癌细胞的生长。使用荧光激活细胞分选分析还观察到，miR-33a的过表达导致A549和NCI-H460细胞系出现明显的G1/S期细胞周期阻滞。蛋白质印迹分析显示，miR-33a的过表达显著降低了A549和NCI-H460细胞中β-连环蛋白的表达，提示miR-33a在肺癌细胞中对β-连环蛋白有直接或间接调控作用。总之，本研究可能为肺癌治疗提供策略并阐明其进展机制。
