Metformin inhibits lung cancer cells proliferation through repressing microRNA-222

Yuqi Wang*, Weimin Dai, Xiangyang Chu, Bo Yang, Ming Zhao, Yu'e Sun

*Corresponding author for this work

Research output: Contribution to journalJournal Articlepeer-review

33 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)2013-2019
Number of pages7
JournalBiotechnology Letters
Volume35
Issue number12
DOIs
Publication statusPublished - Dec 2013
Externally publishedYes

Keywords

  • AMP-activated protein kinase
  • Cancer risk
  • Lung cancer
  • Metformin
  • MicroRNA-222
  • Protein kinase
  • Treatment of lung cancer

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