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

Abstract 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 res...

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Main Authors: Yuhui Han, Wenjiong Sheng, Xiuxin Liu, Haide Liu, Xinyu Jia, Honghui Li, Changyuan Wang, Bin Wang, Tao Hu, Yanchao Ma
Format: Article
Language:English
Published: Nature Portfolio 2024-10-01
Series:Scientific Reports
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Online Access:https://doi.org/10.1038/s41598-024-76155-w
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author Yuhui Han
Wenjiong Sheng
Xiuxin Liu
Haide Liu
Xinyu Jia
Honghui Li
Changyuan Wang
Bin Wang
Tao Hu
Yanchao Ma
author_facet Yuhui Han
Wenjiong Sheng
Xiuxin Liu
Haide Liu
Xinyu Jia
Honghui Li
Changyuan Wang
Bin Wang
Tao Hu
Yanchao Ma
author_sort Yuhui Han
collection DOAJ
description Abstract 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.
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institution OA Journals
issn 2045-2322
language English
publishDate 2024-10-01
publisher Nature Portfolio
record_format Article
series Scientific Reports
spelling doaj-art-0cf42e116e3c44ee8e9fcb2a2c823d082025-08-20T02:11:17ZengNature PortfolioScientific Reports2045-23222024-10-0114111310.1038/s41598-024-76155-wGlycyrrhizin ameliorates colorectal cancer progression by regulating NHEJ pathway through inhibiting HMGB1-induced DNA damage responseYuhui Han0Wenjiong Sheng1Xiuxin Liu2Haide Liu3Xinyu Jia4Honghui Li5Changyuan Wang6Bin Wang7Tao Hu8Yanchao Ma9Department of Immunology, Binzhou Medical UniversityDepartment of Radiotherapy, Yantaishan Hospital, Affiliated Hospital of Binzhou Medical UniversityDepartment of Immunology, Binzhou Medical UniversityDepartment of Radiotherapy, Yantaishan Hospital, Affiliated Hospital of Binzhou Medical UniversityDepartment of Immunology, Binzhou Medical UniversityDepartment of Immunology, Binzhou Medical UniversityDepartment of Immunology, Binzhou Medical UniversityDepartment of Immunology, Binzhou Medical UniversityDepartment of Immunology, Binzhou Medical UniversityDepartment of Immunology, Binzhou Medical UniversityAbstract 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.https://doi.org/10.1038/s41598-024-76155-wColorectal cancer (CRC)Glycyrrhizin (GL)HMGB1DNA damage response (DDR)NHEJ
spellingShingle Yuhui Han
Wenjiong Sheng
Xiuxin Liu
Haide Liu
Xinyu Jia
Honghui Li
Changyuan Wang
Bin Wang
Tao Hu
Yanchao Ma
Glycyrrhizin ameliorates colorectal cancer progression by regulating NHEJ pathway through inhibiting HMGB1-induced DNA damage response
Scientific Reports
Colorectal cancer (CRC)
Glycyrrhizin (GL)
HMGB1
DNA damage response (DDR)
NHEJ
title Glycyrrhizin ameliorates colorectal cancer progression by regulating NHEJ pathway through inhibiting HMGB1-induced DNA damage response
title_full Glycyrrhizin ameliorates colorectal cancer progression by regulating NHEJ pathway through inhibiting HMGB1-induced DNA damage response
title_fullStr Glycyrrhizin ameliorates colorectal cancer progression by regulating NHEJ pathway through inhibiting HMGB1-induced DNA damage response
title_full_unstemmed Glycyrrhizin ameliorates colorectal cancer progression by regulating NHEJ pathway through inhibiting HMGB1-induced DNA damage response
title_short Glycyrrhizin ameliorates colorectal cancer progression by regulating NHEJ pathway through inhibiting HMGB1-induced DNA damage response
title_sort glycyrrhizin ameliorates colorectal cancer progression by regulating nhej pathway through inhibiting hmgb1 induced dna damage response
topic Colorectal cancer (CRC)
Glycyrrhizin (GL)
HMGB1
DNA damage response (DDR)
NHEJ
url https://doi.org/10.1038/s41598-024-76155-w
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