MiR-497 and miR-34a retard lung cancer growth by co-inhibiting cyclin E1 (CCNE1)

Zhiyuan Han, Yanbin Zhang, Qiaoyuan Yang, Binbin Liu, Jianjun Wu, Yajie Zhang, Chengfeng Yang, Yiguo Jiang

Research output: Contribution to journalArticlepeer-review

64 Scopus citations

Abstract

Cyclin E1, encoded by the CCNE1 gene, promotes G1/S transition, chromosome instability, and oncogenesis. Here, we show that miR-497 and miR-34a target the 3'-UTR of CCNE1. miR-497 and miR-34a are downregulated in cancer cells and their ectopic expression inhibited cell proliferation and colony formation in vitro, and inhibited tumor growth in a xenograft model. The effect of simultaneous overexpression of miR-497 and miR-34a on the inhibition of cell proliferation, colony formation, and tumor growth, and the downregulation of cyclin E1 was stronger than the effect of each miRNA alone. The synergistic actions of miR-497 and miR-34a partly correlated with cyclin E1 levels. When cells stably expressing CCNE1 were transfected with the Hi-miR-497/34a plasmid, there was no effect on colony formation, compared with that of cells transfected with either Hi-miR497 or HimiR34a. These results indicate cyclin E1 is downregulated by both miR-497 and miR-34a, which synergistically retard the growth of human lung cancer cells.

Original languageEnglish
Pages (from-to)13149-13163
Number of pages15
JournalOncotarget
Volume6
Issue number15
DOIs
StatePublished - 2015

Keywords

  • CCNE1
  • Lung cancer
  • MiR-34a
  • MiR-497

ASJC Scopus subject areas

  • Oncology

Fingerprint

Dive into the research topics of 'MiR-497 and miR-34a retard lung cancer growth by co-inhibiting cyclin E1 (CCNE1)'. Together they form a unique fingerprint.

Cite this