The Mechanism of Rac1 in Regulating HCC Cell Glycolysis Which Provides Underlying Therapeutic Target for HCC Therapy

Aim. To explore the role of Rac1 on sorafenib resistance in hepatocellular carcinoma. Methods. CCK-8, wound healing assay, Transwell, and cell cycle assay were used to detect the tumor cells development. Cell viability was assessed by MTT. The glycolytic pathway was revealed by cellular metabolism a...

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Published inJournal of oncology Vol. 2022; pp. 1 - 15
Main Authors Ren, Yin-Xiang, Li, Xiao-Bin, Liu, Wei, Yang, Xu-Guang, Liu, Xin, Luo, Yu
Format Journal Article
LanguageEnglish
Published New York Hindawi 06.07.2022
John Wiley & Sons, Inc
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Abstract Aim. To explore the role of Rac1 on sorafenib resistance in hepatocellular carcinoma. Methods. CCK-8, wound healing assay, Transwell, and cell cycle assay were used to detect the tumor cells development. Cell viability was assessed by MTT. The glycolytic pathway was revealed by cellular metabolism assays. Result. We recovered that Rac1 upregulation was related to HCC patients’ poorer prognosis. Forced expression of Rac1 promoted cell development and sorafenib chemoresistance in HCC cells. Rac1 inhibitor EHop-016 and sorafenib combination markedly prevented cell viability, G2/M phase cycle arrest, and apoptosis than single therapy. Furthermore, combination therapy decreased glycolysis in HCC cells. In vivo, the tumor growth was significantly prevented by combination therapy single therapy. Conclusion. Our research declares that Rac1 inhibition could block sorafenib resistance in HCC by decreasing glycolysis, which would provide an underlying target for HCC therapy.
AbstractList Aim. To explore the role of Rac1 on sorafenib resistance in hepatocellular carcinoma. Methods. CCK-8, wound healing assay, Transwell, and cell cycle assay were used to detect the tumor cells development. Cell viability was assessed by MTT. The glycolytic pathway was revealed by cellular metabolism assays. Result. We recovered that Rac1 upregulation was related to HCC patients’ poorer prognosis. Forced expression of Rac1 promoted cell development and sorafenib chemoresistance in HCC cells. Rac1 inhibitor EHop-016 and sorafenib combination markedly prevented cell viability, G2/M phase cycle arrest, and apoptosis than single therapy. Furthermore, combination therapy decreased glycolysis in HCC cells. In vivo, the tumor growth was significantly prevented by combination therapy single therapy. Conclusion. Our research declares that Rac1 inhibition could block sorafenib resistance in HCC by decreasing glycolysis, which would provide an underlying target for HCC therapy.
To explore the role of Rac1 on sorafenib resistance in hepatocellular carcinoma.AimTo explore the role of Rac1 on sorafenib resistance in hepatocellular carcinoma.CCK-8, wound healing assay, Transwell, and cell cycle assay were used to detect the tumor cells development. Cell viability was assessed by MTT. The glycolytic pathway was revealed by cellular metabolism assays.MethodsCCK-8, wound healing assay, Transwell, and cell cycle assay were used to detect the tumor cells development. Cell viability was assessed by MTT. The glycolytic pathway was revealed by cellular metabolism assays.We recovered that Rac1 upregulation was related to HCC patients' poorer prognosis. Forced expression of Rac1 promoted cell development and sorafenib chemoresistance in HCC cells. Rac1 inhibitor EHop-016 and sorafenib combination markedly prevented cell viability, G2/M phase cycle arrest, and apoptosis than single therapy. Furthermore, combination therapy decreased glycolysis in HCC cells. In vivo, the tumor growth was significantly prevented by combination therapy single therapy.ResultWe recovered that Rac1 upregulation was related to HCC patients' poorer prognosis. Forced expression of Rac1 promoted cell development and sorafenib chemoresistance in HCC cells. Rac1 inhibitor EHop-016 and sorafenib combination markedly prevented cell viability, G2/M phase cycle arrest, and apoptosis than single therapy. Furthermore, combination therapy decreased glycolysis in HCC cells. In vivo, the tumor growth was significantly prevented by combination therapy single therapy.Our research declares that Rac1 inhibition could block sorafenib resistance in HCC by decreasing glycolysis, which would provide an underlying target for HCC therapy.ConclusionOur research declares that Rac1 inhibition could block sorafenib resistance in HCC by decreasing glycolysis, which would provide an underlying target for HCC therapy.
Audience Academic
Author Yang, Xu-Guang
Liu, Xin
Liu, Wei
Luo, Yu
Ren, Yin-Xiang
Li, Xiao-Bin
AuthorAffiliation 1 School of Basic Medical Sciences, Lanzhou University, Lanzhou 730000, China
2 School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 100029, China
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Snippet Aim. To explore the role of Rac1 on sorafenib resistance in hepatocellular carcinoma. Methods. CCK-8, wound healing assay, Transwell, and cell cycle assay were...
To explore the role of Rac1 on sorafenib resistance in hepatocellular carcinoma.AimTo explore the role of Rac1 on sorafenib resistance in hepatocellular...
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SubjectTerms Apoptosis
Cancer therapies
Drug resistance
Glucose metabolism
Health aspects
Inhibitor drugs
Leukemia
Liver cancer
Lung cancer
Medical prognosis
Metastasis
Patients
Physiological aspects
Proteins
Stem cells
Targeted cancer therapy
Tumors
Wound healing
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Title The Mechanism of Rac1 in Regulating HCC Cell Glycolysis Which Provides Underlying Therapeutic Target for HCC Therapy
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