Plexin-B1 is a target of miR-214 in cervical cancer and promotes the growth and invasion of HeLa cells
pmid: 21216304
Plexin-B1 is a target of miR-214 in cervical cancer and promotes the growth and invasion of HeLa cells
Plexin-B1, the receptor for Sema4D, has been reported to trigger multiple and sometimes opposing cellular responses in various types of tumor cells. It has been implicated in the regulation of tumor-cell survival, proliferation, angiogenesis, invasion and metastasis. However, the plexin-B1 gene expression and its regulatory mechanism in cervical cancer remain unclear. The present study shows that plexin-B1 is over-expressed in cervical tumor tissues compared to normal cervical tissues by immunohistochemistry, Western blotting and quantitative RT-PCR. The expression of plexin-B1 is significantly associated with cervical tumor metastasis and invasion according to the analysis of the clinicopathologic data. Plexin-B1 also promotes proliferation, migration and invasion in human cervical cancer HeLa cells. We also found that the plexin-B1 levels are inversely correlated with miR-214 amounts in both cervical cancer tissues and HeLa cells. And miR-214 expression level is also associated with metastasis and invasion of cervical tumor. Furthermore, we demonstrate that plexin-B1 is inhibited by miR-214 through a miR-214 binding site within the 3'UTR of plexin-B1 in HeLa cells. Ectopic expression of miR-214 could inhibit the proliferation capacity, migration and invasion ability of HeLa cells. Our findings suggest that plexin-B1, a target of miR-214, may function as an oncogene in human cervical cancer HeLa cells.
- Tianjin Medical University China (People's Republic of)
Base Sequence, Uterine Cervical Neoplasms, Nerve Tissue Proteins, Receptors, Cell Surface, Up-Regulation, Gene Expression Regulation, Neoplastic, MicroRNAs, Cell Movement, Gene Knockdown Techniques, Humans, Female, Neoplasm Invasiveness, Cell Proliferation, HeLa Cells
Base Sequence, Uterine Cervical Neoplasms, Nerve Tissue Proteins, Receptors, Cell Surface, Up-Regulation, Gene Expression Regulation, Neoplastic, MicroRNAs, Cell Movement, Gene Knockdown Techniques, Humans, Female, Neoplasm Invasiveness, Cell Proliferation, HeLa Cells
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