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Rac1调控肝癌细胞糖酵解的机制为肝癌治疗提供潜在治疗靶点

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

作者信息

Ren Yin-Xiang, Li Xiao-Bin, Liu Wei, Yang Xu-Guang, Liu Xin, Luo Yu

机构信息

School of Basic Medical Sciences, Lanzhou University, Lanzhou 730000, China.

School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 100029, China.

出版信息

J Oncol. 2022 Jul 6;2022:7319641. doi: 10.1155/2022/7319641. eCollection 2022.

DOI:10.1155/2022/7319641
PMID:35847360
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9279021/
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.

摘要

目的

探讨Rac1在肝细胞癌索拉非尼耐药中的作用。

方法

采用CCK-8、伤口愈合试验、Transwell和细胞周期试验检测肿瘤细胞的发育情况。通过MTT评估细胞活力。通过细胞代谢试验揭示糖酵解途径。

结果

我们发现Rac1上调与肝癌患者较差的预后相关。Rac1的强制表达促进了肝癌细胞的生长和对索拉非尼的化学抗性。Rac1抑制剂EHop-016与索拉非尼联合使用比单一疗法显著抑制细胞活力、G2/M期细胞周期阻滞和细胞凋亡。此外，联合治疗降低了肝癌细胞的糖酵解。在体内，联合治疗比单一疗法显著抑制肿瘤生长。

结论

我们的研究表明，抑制Rac1可通过降低糖酵解来阻断肝癌对索拉非尼的耐药性，这将为肝癌治疗提供一个潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b2c/9279021/9f9010d30f32/JO2022-7319641.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b2c/9279021/527a10837254/JO2022-7319641.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b2c/9279021/c5bd701dab33/JO2022-7319641.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b2c/9279021/d75aec7e8627/JO2022-7319641.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b2c/9279021/649b0d7255f7/JO2022-7319641.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b2c/9279021/180a02d318e5/JO2022-7319641.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b2c/9279021/c5efd3b0f251/JO2022-7319641.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b2c/9279021/9f9010d30f32/JO2022-7319641.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b2c/9279021/527a10837254/JO2022-7319641.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b2c/9279021/c5bd701dab33/JO2022-7319641.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b2c/9279021/d75aec7e8627/JO2022-7319641.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b2c/9279021/649b0d7255f7/JO2022-7319641.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b2c/9279021/180a02d318e5/JO2022-7319641.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b2c/9279021/c5efd3b0f251/JO2022-7319641.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b2c/9279021/9f9010d30f32/JO2022-7319641.007.jpg

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Gut. 2021 Jul;70(7):1362-1374. doi: 10.1136/gutjnl-2020-321454. Epub 2020 Oct 26.
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RhoA and Rac1 in Liver Cancer Cells: Induction of Overexpression Using Mechanical Stimulation.
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Emerging roles and the regulation of aerobic glycolysis in hepatocellular carcinoma.有氧糖酵解在肝细胞癌中的新兴作用和调控。
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