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Article Abstract
Background. We previously found that expression of SET gene was up-regulated in polycystic ovaries by using microarray. It suggested that SET may be an attractive candidate regulator involved in the pathophysiology of polycystic ovary syndrome (PCOS). In this study, expression and cellular localization of SET protein were investigated in human polycystic and normal ovaries. Method. Ovarian tissues, six normal ovaries and six polycystic ovaries, were collected during transsexual operation and surgical treatment with the signed consent form. The cellular localization of SET protein was observed by immunohistochemistry. The expression levels of SET protein were analyzed by Western Blot. Result. SET protein was expressed predominantly in the theca cells and oocytes of human ovarian follicles in both PCOS ovarian tissues and normal ovarian tissues. The level of SET protein expression in polycystic ovaries was triple higher than that in normal ovaries (P < 0.05). Conclusion. SET was overexpressed in polycystic ovaries more than that in normal ovaries. Combined with its localization in theca cells, SET may participate in regulating ovarian androgen biosynthesis and the pathophysiology of hyperandrogenism in PCOS.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3686144 | PMC |
| http://dx.doi.org/10.1155/2013/367956 | DOI Listing |
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Article Synopsis
- PP2A is a tumor suppressor protein that plays a crucial role in regulating various cellular functions and maintaining cell survival.
- Endogenous inhibitors like CIP2A and SET undermine PP2A's ability to suppress tumors, leading to cancer development and resistance to treatment.
- Interestingly, using external small molecule inhibitors of PP2A can actually boost cancer treatment effectiveness, offering new strategies for tackling drug-resistant tumors and meriting further research.