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- W4311673453 abstract "JUNB transcription factor contributes to the formation of the ubiquitous transcriptional complex AP-1 involved in the control of many physiological and disease-associated functions. The roles of JUNB in the control of cell division and tumorigenic processes are acknowledged but still unclear.Here, we report the results of combined transcriptomic, genomic, and functional studies showing that JUNB promotes cell cycle progression via induction of cyclin E1 and repression of transforming growth factor (TGF)-β2 genes. We also show that high levels of JUNB switch the response of TGF-β2 stimulation from an antiproliferative to a pro-invasive one, induce endogenous TGF-β2 production by promoting TGF-β2 mRNA translation, and enhance tumor growth and metastasis in mice. Moreover, tumor genomic data indicate that JUNB amplification associates with poor prognosis in breast and ovarian cancer patients.Our results reveal novel functions for JUNB in cell proliferation and tumor aggressiveness through regulation of cyclin E1 and TGF-β2 expression, which might be exploited for cancer prognosis and therapy." @default.
- W4311673453 created "2022-12-28" @default.
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- W4311673453 date "2022-12-09" @default.
- W4311673453 modified "2023-10-17" @default.
- W4311673453 title "New roles for AP-1/JUNB in cell cycle control and tumorigenic cell invasion via regulation of cyclin E1 and TGF-β2" @default.
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- W4311673453 doi "https://doi.org/10.1186/s13059-022-02800-0" @default.
- W4311673453 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36494864" @default.
- W4311673453 hasPublicationYear "2022" @default.
- W4311673453 type Work @default.