期刊
ONCOGENE
卷 31, 期 36, 页码 4067-4075出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/onc.2011.561
关键词
miR-133b; tumorigenesis and metastasis; signal pathways; cervical carcinoma
资金
- National High-tech Program of China [2006AA020701, 2009AA022701]
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. Oncogene (2012) 31, 4067-4075; doi: 10.1038/onc.2011.561; published online 19 December 2011
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