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-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.
journal_name
Cancer Lettjournal_title
Cancer lettersauthors
Kim SJ,Saeidi S,Cho NC,Kim SH,Lee HB,Han W,Noh DY,Surh YJdoi
10.1016/j.canlet.2020.11.047subject
Has Abstractpub_date
2021-03-01 00:00:00pages
147-160eissn
0304-3835issn
1872-7980pii
S0304-3835(20)30645-5journal_volume
500pub_type
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