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• W1559905182 abstract "MDM2 and p53 form a negative feedback loop, in which p53 as a transcription factor positively regulates MDM2 and MDM2 negatively regulates tumor suppressor p53 through promoting its degradation. However, the mechanism of the feedback loop is poorly understood in cancers. We had reported previously that the oncoprotein hepatitis B X-interacting protein (HBXIP) is a key oncoprotein in the development of cancer. Thus, we supposed that HBXIP might be involved in the event. Here, we observed that the expression levels of HBXIP were positively correlated to those of MDM2 in clinical breast cancer tissues. Interestingly, HBXIP was able to up-regulate MDM2 at the levels of mRNA and protein in MCF-7 breast cancer cells. Mechanically, HBXIP increased the promoter activities of MDM2 through directly binding to p53 in the P2 promoter of MDM2. Strikingly, we identified that the acetyltransferase p300 was recruited by HBXIP to p53 in the promoter of MDM2. Moreover, we validated that HBXIP enhanced the p53 degradation mediated by MDM2. Functionally, the knockdown of HBXIP or/and p300 inhibited the proliferation of breast cancer cells in vitro, and the depletion of MDM2 or overexpression of p53 significantly blocked the HBXIP-promoted growth of breast cancer in vitro and in vivo. Thus, we concluded that highly expressed HBXIP accelerates the MDM2-mediated degradation of p53 in breast cancer through modulating the feedback loop of MDM2/p53, resulting in the fast growth of breast cancer cells. Our findings provide new insights into the mechanism of the acceleration of the MDM2/p53 feedback loop in the development of cancer. MDM2 and p53 form a negative feedback loop, in which p53 as a transcription factor positively regulates MDM2 and MDM2 negatively regulates tumor suppressor p53 through promoting its degradation. However, the mechanism of the feedback loop is poorly understood in cancers. We had reported previously that the oncoprotein hepatitis B X-interacting protein (HBXIP) is a key oncoprotein in the development of cancer. Thus, we supposed that HBXIP might be involved in the event. Here, we observed that the expression levels of HBXIP were positively correlated to those of MDM2 in clinical breast cancer tissues. Interestingly, HBXIP was able to up-regulate MDM2 at the levels of mRNA and protein in MCF-7 breast cancer cells. Mechanically, HBXIP increased the promoter activities of MDM2 through directly binding to p53 in the P2 promoter of MDM2. Strikingly, we identified that the acetyltransferase p300 was recruited by HBXIP to p53 in the promoter of MDM2. Moreover, we validated that HBXIP enhanced the p53 degradation mediated by MDM2. Functionally, the knockdown of HBXIP or/and p300 inhibited the proliferation of breast cancer cells in vitro, and the depletion of MDM2 or overexpression of p53 significantly blocked the HBXIP-promoted growth of breast cancer in vitro and in vivo. Thus, we concluded that highly expressed HBXIP accelerates the MDM2-mediated degradation of p53 in breast cancer through modulating the feedback loop of MDM2/p53, resulting in the fast growth of breast cancer cells. Our findings provide new insights into the mechanism of the acceleration of the MDM2/p53 feedback loop in the development of cancer." @default.
• W1559905182 created "2016-06-24" @default.
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• W1559905182 date "2015-09-01" @default.
• W1559905182 modified "2023-10-15" @default.
• W1559905182 title "The Oncoprotein HBXIP Modulates the Feedback Loop of MDM2/p53 to Enhance the Growth of Breast Cancer" @default.
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• W1559905182 cites W1963872465 @default.
• W1559905182 cites W1964095007 @default.
• W1559905182 cites W1965381596 @default.
• W1559905182 cites W1966714888 @default.
• W1559905182 cites W1966763036 @default.
• W1559905182 cites W1973714585 @default.
• W1559905182 cites W1973836920 @default.
• W1559905182 cites W1975014056 @default.
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• W1559905182 cites W1998039234 @default.
• W1559905182 cites W2004067791 @default.
• W1559905182 cites W2007098353 @default.
• W1559905182 cites W2014139160 @default.
• W1559905182 cites W2014304644 @default.
• W1559905182 cites W2015704170 @default.
• W1559905182 cites W2016802652 @default.
• W1559905182 cites W2025827059 @default.
• W1559905182 cites W2026907678 @default.
• W1559905182 cites W2034982440 @default.
• W1559905182 cites W2036891904 @default.
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• W1559905182 cites W2050455358 @default.
• W1559905182 cites W2052130151 @default.
• W1559905182 cites W2053844022 @default.
• W1559905182 cites W2056530510 @default.
• W1559905182 cites W2056713498 @default.
• W1559905182 cites W2058737236 @default.
• W1559905182 cites W2059044416 @default.
• W1559905182 cites W2060765541 @default.
• W1559905182 cites W2064330613 @default.
• W1559905182 cites W2078149279 @default.
• W1559905182 cites W2082979850 @default.
• W1559905182 cites W2087769276 @default.
• W1559905182 cites W2089082314 @default.
• W1559905182 cites W2094268500 @default.
• W1559905182 cites W2102930268 @default.
• W1559905182 cites W2103237568 @default.
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• W1559905182 cites W2111957657 @default.
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• W1559905182 doi "https://doi.org/10.1074/jbc.m115.658468" @default.
• W1559905182 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4566238" @default.
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• W1559905182 hasPublicationYear "2015" @default.
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