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Oncoprotein HBXIP induces PKM2 via transcription factor E2F1 to promote cell proliferation in ER-positive breast cancer by Liu, Bo-wen; Wang, Tian-jiao; Li, Lei-lei; Zhang, Lu; Liu, Yun-xia; Feng, Jin-yan; Wu, Yue; Xu, Fei-fei; Zhang, Quan-sheng; Bao, Ming-zhu; Zhang, Wei-ying; Ye, Li-hong is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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We have reported that hepatitis B X-interacting protein (HBXIP, also termed LAMTOR5) can act as an oncogenic transcriptional co-activator to modulate gene expression, promoting breast cancer development. Pyruvate kinase muscle isozyme M2 (PKM2), encoded by PKM gene, has emerged as a key oncoprotein in breast cancer. Yet, the regulatory mechanism of PKM2 is still unexplored. Here, we report that HBXIP can upregulate PKM2 to accelerate proliferation of estrogen receptor positive (ER+) breast cancer. Immunohistochemistry analysis using breast cancer tissue microarray uncovered a positive association between the expression of HBXIP and PKM2. We also discovered that PKM2 expression was positively related with HBXIP expression in clinical breast cancer patients by real-time PCR assay. Interestingly, in ER+ breast cancer cells, HBXIP was capable of upregulating PKM2 expression at mRNA and protein levels in a dose-dependent manner, as well as increasing the activity of PKM promoter. Mechanistically, HBXIP could stimulate PKM promoter through binding to the -779/-579 promoter region involving co-activation of E2F transcription factor 1 (E2F1). In function, cell viability, EdU, colony format

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Author

Liu, Bo-wen; Wang, Tian-jiao; Li, Lei-lei; Zhang, Lu; Liu, Yun-xia; Feng, Jin-yan; Wu, Yue; Xu, Fei-fei; Zhang, Quan-sheng; Bao, Ming-zhu; Zhang, Wei-ying; Ye, Li-hong

Publisher

Nature Publishing Group; Springer Science and Business Media LLC (ISSN 1671-4083)

Published

2018

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)