Abstract | BACKGROUND: METHODS: We analyzed gene expression in 20 specimens each of human HCC and normal liver tissue by quantitative real-time PCR and immunohistochemistry. Proliferation was analyzed by foci formation and senescence by β- galactosidase staining. Promoter activity was detected by luciferase reporter assay. RESULTS: The expression of RBP2 was stronger in cancerous than non-cancerous tissues, but that of its binding microRNA, Homo sapiens miR-212 (hsa-miR-212), showed an opposite pattern. SiRNA knockdown of RBP2 significantly upregulated cyclin-dependent kinase inhibitors (CDKIs), with suppression of HCC cell proliferation and induction of senescence. Overexpression of hsa-miR-212 suppressed RBP2 expression, with inhibited cell proliferation and induced cellular senescence, which coincided with upregulated CDKIs; with low hsa-miR-212 expression, CDKIs were downregulated in HCC tissue. Inhibition of hsa-miR-212 expression upregulated RBP2 expression. Luciferase reporter assay detected the direct binding of hsa-miR-212 to the RBP2 3' UTR. CONCLUSIONS: RBP2 is overexpressed in HCC and negatively regulated by hsa-miR-212. The hsa-miR-212-RBP2-CDKI pathway may be important in the pathogenesis of HCC.
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Authors | Xiuming Liang, Jiping Zeng, Lixiang Wang, Ming Fang, Qing Wang, Min Zhao, Xia Xu, Zhifang Liu, Wenjuan Li, Shili Liu, Han Yu, Jihui Jia, Chunyan Chen |
Journal | PloS one
(PLoS One)
Vol. 8
Issue 7
Pg. e69784
( 2013)
ISSN: 1932-6203 [Electronic] United States |
PMID | 23922798
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- MicroRNAs
- Retinoblastoma-Binding Protein 2
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Topics |
- Adult
- Aged
- Carcinoma, Hepatocellular
(genetics, metabolism)
- Female
- Humans
- Immunohistochemistry
- Liver
- Male
- MicroRNAs
(genetics)
- Middle Aged
- Real-Time Polymerase Chain Reaction
- Retinoblastoma-Binding Protein 2
(genetics, metabolism)
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