MicroRNA-133b is a key promoter of cervical carcinoma development through the activation of the ERK and AKT1 pathways

W. Qin, P. Dong, C. Ma, K. Mitchelson, T. Deng, L. Zhang, Y. Sun, X. Feng, Y. Ding, X. Lu, J. He, H. Wen, J. Cheng

Research output: Contribution to journalArticlepeer-review

101 Scopus citations


We report that elevated microRNA-133b (miR-133b) acts as an oncogene in human cervical carcinoma to promote tumorigenesis and metastasis. In situ hybridization confirmed that miR-133b is localized in proliferating human cervical carcinoma cells with levels progressively elevating throughout advancing stages. Cellular studies showed that miR-133b enhances cell proliferation and colony formation by targeting mammalian sterile 20-like kinase 2 (MST2), cell division control protein 42 homolog (CDC42) and ras homolog gene family member A (RHOA), which subsequently results in activation of the tumorigenic protein kinase B alpha (AKT1) and mitogen-activated protein kinase (ERK1 and ERK2, here abbreviated as ERK) signaling pathways. Mouse experiments revealed that upregulation of miR-133b in cervical carcinoma cells strongly promotes both in vivo tumorigenesis and independent metastasis to the mouse lung. The data indicates that upregulation of miR-133b shortens the latency of cervical carcinoma. Together, these findings suggest that miR-133b could be a potent marker for the early onset of cervical carcinoma.

Original languageEnglish (US)
Pages (from-to)4067-4075
Number of pages9
Issue number36
StatePublished - Sep 6 2012


  • cervical carcinoma
  • miR-133b
  • signal pathways
  • tumorigenesis and metastasis

ASJC Scopus subject areas

  • Molecular Biology
  • Cancer Research
  • Genetics


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