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

Su Jung Kim, Soma Saeidi, Nam Chul Cho, Seung Hyeon Kim, Han Byoel Lee, Wonshik Han, Dong Young Noh, Young Joon Surh

Research output: Contribution to journalArticlepeer-review

1 Scopus citations


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.

Original languageEnglish
Pages (from-to)147-160
Number of pages14
JournalCancer Letters
StatePublished - 1 Mar 2021


  • Breast cancer
  • IL-23A
  • Nrf2
  • STAT3

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