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Abstract
<p class="first" id="d2853905e153">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-STAT3Y705
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.
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