Glycyrrhizin ameliorates colorectal cancer progression by regulating NHEJ pathway through inhibiting HMGB1-induced DNA damage response.


Journal

Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288

Informations de publication

Date de publication:
23 10 2024
Historique:
received: 08 06 2024
accepted: 10 10 2024
medline: 23 10 2024
pubmed: 23 10 2024
entrez: 22 10 2024
Statut: epublish

Résumé

As one of the most common malignancies, colorectal cancer (CRC) usually starts with a benign lesion and accumulates DNA damage as it progresses to full-fledged cancer. Glycyrrhizin (GL) has been found to alleviate tumor growth and inflammation, while the role of GL influences DNA damage response (DDR) in colorectal cancer remains unclear. GL exposure significantly reduced cell colony formation and viability with a concomitant increase in DNA fragmentation in CRC, meanwhile GL induced apoptosis by activating caspase-3. Moreover, GL induced cell cycle arrest in CRC cells at S phase, which was associated with decreased cyclin D1 in vitro. GL treatment significantly ameliorated tumor growth and promoted DDR in vivo. Mechanism analysis revealed that GL significantly downregulated the NHEJ pathway via inhibiting HMGB1. Finally, the expression of HMGB1 was abnormal regulated in CRC tissue than in adjacent normal tissues and associated with TNM stage and overall survival. Our findings indicate that HMGB1 may be a novel therapeutic target in CRC, a result that GL may serve as a promising drug for CRC treatment.

Identifiants

pubmed: 39438689
doi: 10.1038/s41598-024-76155-w
pii: 10.1038/s41598-024-76155-w
doi:

Substances chimiques

HMGB1 Protein 0
Glycyrrhizic Acid 6FO62043WK
HMGB1 protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

24948

Subventions

Organisme : Medical and Health Science and Technology Project of Shandong Province
ID : 202309030619
Organisme : National Natural Science Foundation of China
ID : 82203543
Organisme : Initial project of Binzhou Medical University
ID : 50012304458
Organisme : Shandong Province Natural Science Foundation
ID : ZR2022QH267

Informations de copyright

© 2024. The Author(s).

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Auteurs

Yuhui Han (Y)

Department of Immunology, Binzhou Medical University, 346 Guanhai Road, Yantai, 264003, Shandong, China.

Wenjiong Sheng (W)

Department of Radiotherapy, Yantaishan Hospital, Affiliated Hospital of Binzhou Medical University, 10087 Science and Technology Avenue, Yantai, 264003, Shandong, China.

Xiuxin Liu (X)

Department of Immunology, Binzhou Medical University, 346 Guanhai Road, Yantai, 264003, Shandong, China.

Haide Liu (H)

Department of Radiotherapy, Yantaishan Hospital, Affiliated Hospital of Binzhou Medical University, 10087 Science and Technology Avenue, Yantai, 264003, Shandong, China.

Xinyu Jia (X)

Department of Immunology, Binzhou Medical University, 346 Guanhai Road, Yantai, 264003, Shandong, China.

Honghui Li (H)

Department of Immunology, Binzhou Medical University, 346 Guanhai Road, Yantai, 264003, Shandong, China.

Changyuan Wang (C)

Department of Immunology, Binzhou Medical University, 346 Guanhai Road, Yantai, 264003, Shandong, China.

Bin Wang (B)

Department of Immunology, Binzhou Medical University, 346 Guanhai Road, Yantai, 264003, Shandong, China.

Tao Hu (T)

Department of Immunology, Binzhou Medical University, 346 Guanhai Road, Yantai, 264003, Shandong, China.

Yanchao Ma (Y)

Department of Immunology, Binzhou Medical University, 346 Guanhai Road, Yantai, 264003, Shandong, China. myc403@bzmc.edu.cn.

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