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

Bokan Chen, Min Zhang, Xia Lin

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Article in International journal of clinical oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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3 authors.

Bokan ChenDepartment of Hepatobiliary and Pancreatic Surgery and Zhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.

Min ZhangDepartment of Hepatobiliary and Pancreatic Surgery and Zhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China. minzh@zju.edu.cn.

Xia LinDepartment of Hepatobiliary and Pancreatic Surgery and Zhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China. xialinzheda@zju.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChromodomain 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). MATERIALS AND

methodsPublic 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.

resultsCHD6 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.

conclusionCHD6 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.

Indexed as

Mi-2 Nucleosome Remodeling and Deacetylase ComplexTriple Negative Breast NeoplasmsAnimalsApoptosisBiomarkers, TumorCell Line, TumorCell MovementCell ProliferationDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansMAP Kinase Signaling SystemMicePhosphatidylinositol 3-KinasesPrognosisBiomarkers, TumorMi-2 Nucleosome Remodeling and Deacetylase ComplexPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktCHD6FGFR3MigrationProliferationTriple-negative breast cancer

Identifiers

PMID42283962

DOI10.3390/ijms232112815

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.