AI Article Synopsis
- Previous research indicates that miR-214 is overexpressed in various cancers, contributing to chemoresistance and metastasis.
- In this study, miR-214 was linked to ovarian cancer stem cell properties by inhibiting the p53/Nanog signaling pathway, showing that higher levels of miR-214 enhance OCSC traits.
- The findings suggest that targeting miR-214 could serve as a potential treatment strategy for ovarian cancer by reversing its effects on OCSC characteristics through p53 regulation.
Article Abstract
Previous studies have shown aberrant expression of miR-214 in human malignancy. Elevated miR-214 is associated with chemoresistance and metastasis. In this study, we identified miR-214 regulation of ovarian cancer stem cell (OCSC) properties by targeting p53/Nanog axis. Enforcing expression of miR-214 increases, whereas knockdown of miR-214 decreases, OCSC population and self-renewal as well as the Nanog level preferentially in wild-type p53 cell lines. Furthermore, we found that p53 is directly repressed by miR-214 and that miR-214 regulates Nanog through p53. Expression of p53 abrogated miR-214-induced OCSC properties. These data suggest the critical role of miR-214 in OCSC via regulation of the p53-Nanog axis and miR-214 as a therapeutic target for ovarian cancer.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3471722 | PMC |
| http://dx.doi.org/10.1074/jbc.M112.374611 | DOI Listing |
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