The multifaceted therapeutic value of targeting steroid receptor coactivator-1 in tumorigenesis.

NCOA1 SRC-1 Steroid hormone Tumour progression

Journal

Cell & bioscience
ISSN: 2045-3701
Titre abrégé: Cell Biosci
Pays: England
ID NLM: 101561195

Informations de publication

Date de publication:
29 Mar 2024
Historique:
received: 24 01 2024
accepted: 22 03 2024
medline: 30 3 2024
pubmed: 30 3 2024
entrez: 30 3 2024
Statut: epublish

Résumé

Steroid receptor coactivator-1 (SRC-1, also known as NCOA1) frequently functions as a transcriptional coactivator by directly binding to transcription factors and recruiting to the target gene promoters to promote gene transcription by increasing chromatin accessibility and promoting the formation of transcriptional complexes. In recent decades, various biological and pathological functions of SRC-1 have been reported, especially in the context of tumorigenesis. SRC-1 is a facilitator of the progression of multiple cancers, including breast cancer, prostate cancer, gastrointestinal cancer, neurological cancer, and female genital system cancer. The emerging multiorgan oncogenic role of SRC-1 is still being studied and may not be limited to only steroid hormone-producing tissues. Growing evidence suggests that SRC-1 promotes target gene expression by directly binding to transcription factors, which may constitute a novel coactivation pattern independent of AR or ER. In addition, the antitumour effect of pharmacological inhibition of SRC-1 with agents including various small molecules or naturally active compounds has been reported, but their practical application in clinical cancer therapy is very limited. For this review, we gathered typical evidence on the oncogenic role of SRC-1, highlighted its major collaborators and regulatory genes, and mapped the potential mechanisms by which SRC-1 promotes primary tumour progression.

Identifiants

pubmed: 38553750
doi: 10.1186/s13578-024-01222-8
pii: 10.1186/s13578-024-01222-8
doi:

Types de publication

Journal Article Review

Langues

eng

Pagination

41

Subventions

Organisme : National Natural Science Foundation of China
ID : 82173086
Organisme : National Natural Science Foundation of China
ID : 82303144
Organisme : Natural Science Foundation of Zhejiang Province
ID : LQ24H160002
Organisme : Natural Science Foundation of Ningbo Municipality
ID : 2023J375
Organisme : Key Laboratory of Precision Medicine for Atherosclerotic Diseases of Zhejiang Province, China
ID : 2022E10026
Organisme : Fund of the Technology Innovation Center for Exploitation of Marine Biological Resources, MNR
ID : TICMBR202301
Organisme : The Keynote Research Project of Ningbo City
ID : 2023Z171

Informations de copyright

© 2024. The Author(s).

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Auteurs

Qiang Chen (Q)

Zhejiang Key Laboratory of Pathophysiology, Department of Biochemistry and Molecular Biology, Health Science Center, Ningbo University, Ningbo, Zhejiang, 315211, China. chenqiang1@nbu.edu.cn.
Key Laboratory of Precision Medicine for Atherosclerotic Diseases of Zhejiang Province, Affiliated First Hospital of Ningbo University, Ningbo, Zhejiang, 315010, China. chenqiang1@nbu.edu.cn.

Peng Guo (P)

Department of Cell Biotechnology Laboratory, Tianjin Cancer Hospital Airport Hospital, Tianjin, 300308, China.
State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian, 361104, China.

Yilin Hong (Y)

State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian, 361104, China.

Pingli Mo (P)

State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian, 361104, China.

Chundong Yu (C)

State Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian, 361104, China. cdyu@xmu.edu.cn.

Classifications MeSH