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Interaction of Nrf2 with dimeric STAT3 induces IL-23 expression: Implications for breast cancer progression

Cited 7 time in Web of Science Cited 4 time in Scopus
Issue Date
2021-03
Citation
Cancer Letters, Vol.500, pp.147-160
Keywords
Nrf2;STAT3;IL-23A;Breast cancer
Abstract
Persistent activation of STAT3 and Nrf2 is considered to stimulate the aggressive behavior of basal-like breast cancer (BLBC). However, the precise mechanism underlying sustained overactivation of these transcription factors and their roles in breast cancer progression remain elusive. Analysis of the TCGA multi-omics data showed that high levels of STAT3 and Nrf2 mRNA were correlated with elevated expression of P-STAT3(Y705) and Nrf2 target proteins in breast cancer patients. Our present study demonstrates a unique interaction between Nrf2 and STAT3 in the maintenance and progression of BLBC. RNA sequencing analysis identified the gene encoding IL-23A upregulated by concurrent binding of STAT3 and Nrf2 to its promoter. IL-23A depletion also showed the similar phenotypic changes to those caused by double knockdown of both transcription factors. In conclusion, the STAT3-Nrf2 interaction accelerates BLBC growth and progression by augmenting IL-23A expression, which underscores the importance of subtype-specific molecular pathways in human breast cancer.Y
ISSN
0304-3835
URI
https://hdl.handle.net/10371/178054
DOI
https://doi.org/10.1016/j.canlet.2020.11.047
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