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• W3112953811 abstract "Abstract B-cell translocation gene 3 ( BTG3 ) is a member of the antiproliferative BTG gene family and is a downstream target of p53. Here, we show that senescence triggered by BTG3 depletion was accompanied by a secretome enriched with cytokines, growth factors, and matrix-remodeling enzymes, which could promote angiogenesis and cell scattering in vitro. We present evidence that at least part of these activities can be explained by elevated HIF-1α activity. Mechanistically, the BTG3 C-terminal domain competes with the coactivator p300 for binding the HIF-1α transactivation domain. The angiogenic promoting effect of BTG3 knockdown was largely diminished upon co-depletion of HIF-1α, indicating that HIF-1α is a major downstream target of BTG3 in the control of angiogenesis. In vivo, ectopic expression of BTG3 suppresses angiogenesis in xenograft tumors; and syngenic tumor growth and metastasis were enhanced in Btg3 -null mice. Moreover, analysis of clinical datasets revealed that a higher BTG3 / VEGFA expression ratio correlates with improved patient survival in a number of cancer types. Taken together, our findings highlight the non-autonomous regulation of tumor microenvironment by BTG3 while suppressing tumor progression." @default.
• W3112953811 created "2020-12-21" @default.
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• W3112953811 date "2020-12-11" @default.
• W3112953811 modified "2023-10-16" @default.
• W3112953811 title "Loss of the tumor suppressor BTG3 drives a pro-angiogenic tumor microenvironment through HIF-1 activation" @default.
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• W3112953811 doi "https://doi.org/10.1038/s41419-020-03248-5" @default.
• W3112953811 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7732837" @default.
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• W3112953811 hasPublicationYear "2020" @default.
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