The DOI matches its Crossref record; 33 of the 33 references it cites were found in a registry or an index.
STAT3 is a potential modulator of HIF‐1‐mediated VEGF expression in human renal carcinoma cells
Abstract
Aberrantly enhanced vascular endothelial growth factor (VEGF) gene expression is associated with increased tumor growth and metastatic spread of solid malignancies, including human renal carcinomas. Persistent activation of STAT3 is linked to tumor‐associated angiogenesis, but underlying mechanisms remain unclear. Therefore, we examined whether STAT3 modulates the stability and activity of hypoxia‐inducible factor‐1α (HIF‐1α), and in turn enhances VEGF expression. We found that STAT3 was activated in ischemic rat kidneys and hypoxic human renal carcinoma cells. We also found that hypoxia‐induced activation of STAT3 transactivated the VEGF promoter and increased the expression of VEGF transcripts. Consistent with these findings, STAT3 inhibition attenuated the hypoxic induction of VEGF. Interestingly, activated STAT3 increased HIF‐1α protein levels due to the HIF‐1α stability by blocking HIF‐1α degradation and accelerated its de novo synthesis. The novel interaction of STAT3 with HIF‐1α was identified in hypoxic renal carcinoma cells. Furthermore, hypoxia recruited STAT3, HIF‐1α, and p300 to the VEGF promoter and induced histone H3 acetylation. Therefore, these findings provide compelling evidence that a causal relationship exists between STAT3 activation and HIF‐1‐dependent angiogenesis and suggest that therapeutic modalities designed to disrupt STAT3 signaling hold considerable promise for the blocking tumor growth and enhancing apoptosis of cancer cells and tissues.
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Cited by
Yang, W., Yu, T., Huang, X., Bilotta, A. J., Xu, L., Lu, Y., Sun, J., Pan, F., Zhou, J., Zhang, W., et al. (2020) · Nature Communications · doi:10.1038/s41467-020-18262-6 · Cited by 1,042
Aggarwal, B. B., Kunnumakkara, A. B., Harikumar, K. B., Gupta, S. R., Tharakan, S. T., Koca, C., Dey, S., & Sung, B. (2009) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2009.04911.x · Cited by 649
Hypoxia, oxidative stress and inflammation
McGarry, T., Biniecka, M., Veale, D. J., & Fearon, U. (2018) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2018.03.042 · Cited by 601
Sun, Q., Chen, X., Ma, J., Peng, H., Wang, F., Zha, X., Wang, Y., Jing, Y., Yang, H., Chen, R., et al. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1014769108 · Cited by 586
HIF‐1 at the crossroads of hypoxia, inflammation, and cancer
Balamurugan, K. (2016) · International Journal of Cancer · doi:10.1002/ijc.29519 · Cited by 572
Metadata
- Authors
- Jung, J. E., Lee, H., Cho, I., Chung, D. H., Yoon, S., Yang, Y. M., Lee, J. W., Choi, S., Park, J., Ye, S., & Chung, M.
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2005-05-26
- Volume
- 19
- Issue
- 10
- Pages
- 1296-1298
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- OpenAlex
- W2123373938
- Cited by
- 425
- References
- 33
- FWCI
- 4.91
- Type
- journal article
- Language
- en
- Open access
- closed
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- Jung, J. E., Lee, H., Cho, I., Chung, D. H., Yoon, S., Yang, Y. M., Lee, J. W., Choi, S., Park, J., Ye, S., & Chung, M. (2005). STAT3 is a potential modulator of HIF‐1‐mediated VEGF expression in human renal carcinoma cells. The FASEB Journal. https://doi.org/10.1096/fj.04-3099fje
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