Department of Thoracic Surgery, General Hospital of the People's Liberation Army, Beijing, 100853, China,
Biotechnol Lett. 2013 Dec;35(12):2013-9. doi: 10.1007/s10529-013-1309-0. Epub 2013 Aug 24.
Metformin, which is commonly used as an oral anti-hyperglycemic agent of the biguanide family, may reduce cancer risk and improve prognosis. However, the mechanism by which metformin affects various cancers, including lung cancer, remains unknown. MiR-222 induces cell growth and cell cycle progression via direct targeting of p27, p57 and PTEN in cancer cells. In the present study, we used A549 and NCI-H358 human lung cancer cell lines to study the effects and mechanisms of metformin. Metformin treatment reduced expression of miR-222 in these cells (p < 0.05). As a result, protein abundance of p27, p57 and PTEN were increased in cells exposed to metformin. Therefore, these data provide novel evidence for a mechanism that may contribute to the anti-neoplastic effects of metformin suggested by recent population studies and justifying further work to explore potential roles for it in lung cancer treatment.
二甲双胍是一种常用的双胍类口服抗高血糖药物，可能降低癌症风险并改善预后。然而，二甲双胍影响包括肺癌在内的各种癌症的机制尚不清楚。miR-222 通过直接靶向癌细胞中的 p27、p57 和 PTEN 诱导细胞生长和细胞周期进程。在本研究中，我们使用 A549 和 NCI-H358 人肺癌细胞系来研究二甲双胍的作用和机制。二甲双胍处理降低了这些细胞中 miR-222 的表达（p<0.05）。结果，暴露于二甲双胍的细胞中 p27、p57 和 PTEN 的蛋白丰度增加。因此，这些数据为最近的人群研究表明的二甲双胍的抗肿瘤作用的机制提供了新的证据，并证明有必要进一步研究其在肺癌治疗中的潜在作用。
