Liang Peng, Limei Liu, Ling Xu, Jie Chen, Xiaohui Wang, Meihua Zhang, Yilong Ge
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引用次数: 0
Abstract
Ovarian cancer is one of the most common and lethal malignancy tumors in women. Chemoresistance is one of the main reasons for ovarian cancer relapsing. Understanding the regulatory mechanisms of chemoresistance generation is critical to develop novel therapeutic strategies. Here, we found that TRIM46 was upregulated in ovarian cancer cells and tissues with chemoresistance and associated with poor outcomes. Functional assays showed that TRIM46 promoted cisplatin (CDDP) chemoresistance. Furthermore, TRIM46 interacts with PI3K/AKT pathway inactivator pleckstrin homology domain leucine-rich repeat protein phosphatase 2 (PHLPP2) and downregulated PHLPP2 level. Treating with PI3K/AKT pathway inhibitor significantly reversed the effects of TRIM46-overexpressing on chemoresistance. In summary, our study reveals that TRIM46 promoted chemoresistance via downregulating PHLPP2, leading to activating PI3K/AKT pathway. This study provides a novel potential target for ovarian cancer therapy.
期刊介绍：
Published since 1929, Biochemistry and Cell Biology explores every aspect of general biochemistry and includes up-to-date coverage of experimental research into cellular and molecular biology in eukaryotes, as well as review articles on topics of current interest and notes contributed by recognized international experts. Special issues each year are dedicated to expanding new areas of research in biochemistry and cell biology.
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