Microrna-23a/27a/24-2 cluster promotes gastric cancer cell proliferation synergistically

Kate Hua, Yu Ting Chen, Chian Feng Chen, Ya Syuan Tang, Tzu Ting Huang, Yu Cheng Lin, Tien Shun Yeh, Kuo Hung Huang, Hsin Chen Lee, Ming Ta Hsu, Chin Wen Chi, Chew Wun Wu, Chi Hung Lin, Yueh Hsin Ping*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

16 Scopus citations

Abstract

Previous studies have indicated that certain microRNAs (miRNAs/miRs) function as either tumor suppressors or oncogenes in human cancer. The present study identified the miR-23a/27a/24-2 cluster, containing miR-23, miR-27a and miR-24, as an oncogene in gastric cancer. The expression of the miR-23a/27a/24-2 cluster was upregulated in clinical gastric cancer tissues. Transfection with inhibitors of miR-23a, miR-27a, or miR-24, either independently or together, repressed in vitro colony formation and in vivo tumor formation. The miR23a/27a/24-2 cluster inhibitors repressed the growth of gastric cancer cells in a synergistic manner. In addition, treatment with lower doses of the miRNA inhibitor mixture induced the formation of apoptotic bodies. According to computational predictions using TargetScan, suppressor of cytokine-induced signaling 6 (SOCS6) was identified as one of the downstream target genes of the miR-23a/27a/24-2 cluster. The expression of SOCS6 was significantly lower in tumor tissues than in matched normal tissues (P<0.01) and was associated with poor survival (P<0.00001). Taken together, these results strongly suggested that the miR-23a/27a/24-2 cluster may mediate the progression of gastric cancer through the suppression of SOCS6 expression. The present study also provides a novel molecular target for the development of an anti-gastric cancer agent.

Original languageEnglish
Pages (from-to)2319-2325
Number of pages7
JournalOncology Letters
Volume16
Issue number2
DOIs
StatePublished - Aug 2018

Keywords

  • Gastric cancer
  • MicroRNA-23a/27a/24-2 cluster
  • Suppressor of cytokine-induced signaling 6

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