SDCBP/Syntenin-1 stabilizes BACH1 by disassembling the SCF^FBXO22-BACH1 complex in triple-negative breast cancer.

ABSTRACT: BACH1 is a redox-sensitive transcription factor facilitating tumor progression in triple-negative breast cancer (TNBC). However, the molecular mechanisms regulating BACH1 function in TNBC remain unclear. In this study, we demonstrate that SDCBP, a tandem-PDZ-domain protein, stabilizes BACH1 by disassembling the Skp1-Cullin1-FBXO22 (SCF^FBXO22)-BACH1 complex via a heme/heme-oxygenase-1-independent manner in TNBC cells. Our data revealed that SDCBP and BACH1 expression show a significant positive correlation in TNBC cells and TNBC patients tumor tissues. Mechanistically, SDCBP via its PDZ1 domain disassembles the SCF^FBXO22-BACH1 complex via its PDZ1 domain, thereby preventing BACH1 K48-linked polyubiquitination and proteasomal degradation. Knocking down SDCBP induces BAC

SUBMITTER: Tran PL 

PROVIDER: S-EPMC12130529 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature