CHD6 promotes triple-negative breast cancer progression and is associated with PI3K/AKT and MAPK pathways

Chromodomain helicase DNA-binding protein 6 (CHD6), a member of the CHD family, is involved in chromatin remodeling and transcriptional regulation, yet its role in cancer remains unclear. This study aimed to investigate the biological function and clinical significance of CHD6 in triple-negative breast cancer (TNBC).

Public datasets were analyzed to evaluate CHD6 expression and prognostic value in TNBC. In vitro assays, including cell proliferation, migration, and invasion, were performed following CHD6 knockdown. A xenograft mouse model was used to assess tumor growth in vivo. Transcriptome sequencing was conducted to explore potential downstream mechanisms.

CHD6 expression was significantly upregulated in TNBC tissues and was associated with poor prognosis. CHD6 knockdown markedly inhibited TNBC cell proliferation, migration, and invasion in vitro, and suppressed tumor growth while promoting apoptosis in vivo. Transcriptome analysis suggested that CHD6 downregulation may be associated with altered FGFR3 expression and potential changes in PI3K/AKT and MAPK signaling pathways.

CHD6 promotes TNBC progression by enhancing tumor cell proliferation and survival. It may also be associated with FGFR3-related signaling pathways. These findings suggest that CHD6 may represent a potential prognostic biomarker and candidate therapeutic target in TNBC, although further mechanistic and translational studies are required.