Tumor suppression by miR-31 in esophageal carcinoma is p21- dependent

Zhifeng Ning, Hua Zhu, Feifei Li, Qing Liu, Gefei Liu, Tao Tan, Bo Zhang, Shaobin Chen, Guanwu Li, Dongyang Huang, Stephen J. Meltzer, Hao Zhang

Research output: Contribution to journalArticlepeer-review


microRNA regulation network is important for the cancer genetic heterogeneity. Relative to the increasing numbers of microRNA’s targets identified, upstream regulatory mechanisms that control functional microRNAs are less well-documented. Here, we investigated the function of miR-31, a pleiotropically-acting microRNA, in esophageal squamous cell cancer (ESCC). We demonstrated that miR-31 only exerted tumor-suppressive effects in TE-7 ESCC cells, but not in TE-1 ESCC cells, although both of these cell lines harbor inactive p53. Interestingly, TE-1 cells highly expressed p21, while p21 levels were virtually undetectable in TE-7 cells, suggesting a p21-dependent mechanism of miR-31-mediated tumor suppression. Accordingly, knockdown of p21 in TE-1 cells reversed the tumor suppressive actions of miR-31. In patient ESCC specimens, real-time RT-PCR analysis revealed that expression of E2F2 and STK40, two known miR-31 target oncogenes, was negatively correlated with the expression of miR-31 in a p21-dependent manner, supporting the conclusion that miR-31 only downregulates its target oncogenes when p21 levels are low. Collectively, these data suggest a novel mechanism through which the tumor-suppressive effect of miR-31 is p21-dependent. In addition, we speculate that delivery of miR-31 could provide therapeutic benefit in the personalized management of a subgroup of ESCC patients with p21-deficient tumors.

Original languageEnglish (US)
Pages (from-to)436-444
Number of pages9
JournalGenes and Cancer
Issue number11-12
StatePublished - 2014


  • Esophageal squamous cell cancer
  • MiR-31
  • MicroRNA
  • P21
  • Personalized medicine

ASJC Scopus subject areas

  • Genetics
  • Cancer Research


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