Ginsenoside Rb1 Inhibits the Proliferation of Lung Cancer Cells by Inducing the Mitochondrial-mediated Apoptosis Pathway
- Autores: Feng L.1, Liu X.2, Sun K.2, Sun Y.3, Wu W.2, Chen C.2, Jin X.4, Wan X.2
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Afiliações:
- College of Pharmacy, Changchun University of Chinese Medicine
- Jilin Ginseng Academy, Changchun University of Chinese Medicine
- , The Second Hospital of Dalian Medical University
- Key Laboratory of Molecular Epigenetics of the Ministry of Education (MOE), Northeast Normal University
- Edição: Volume 24, Nº 12 (2024)
- Páginas: 928-941
- Seção: Oncology
- URL: https://snv63.ru/1871-5206/article/view/643780
- DOI: https://doi.org/10.2174/0118715206299212240304142047
- ID: 643780
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Resumo
Background:Lung cancer is one of the more common malignant tumors posing a great threat to human life, and it is very urgent to find safe and effective therapeutic drugs. The antitumor effect of ginsenosides has been reported to be a treatment with a strong effect and a high safety profile.
Objective:This paper aimed to investigate the inhibitory effect of ginsenoside Rb1 on 95D and NCI-H460 lung cancer cells and its pathway to promote apoptosis.
Methods:We performed the CCK-8 assay, fluorescence staining assay, flow cytometry, scratch healing assay, and Transwell assay to detect the effects of different concentrations of ginsenoside Rb1 on the antitumor activity of 95D and NCI-H460 cells and Western Blot detected the mechanism of antitumor effect.
Results:Ginsenoside Rb1 treatment significantly increased the inhibition and apoptosis rates of 95D and NCIH460 cells and inhibited the cell cycle transition from S phase to G2/M. Rb1 induces apoptosis by altering the levels of P53, Bax, Cyto-c, Caspase-8, Caspase-3, Cleaved Caspase-3, Bcl-2, MMP-2, and MMP-9 proteins and activating the external apoptotic pathway.
Conclusion:Ginsenoside Rb1 inhibits proliferation and migration and induces apoptosis of 95D and NCI-H460 lung cancer cells by regulating the mitochondrial apoptotic pathway to achieve antitumor activity.
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Sobre autores
Lin Feng
College of Pharmacy, Changchun University of Chinese Medicine
Email: info@benthamscience.net
Xinze Liu
Jilin Ginseng Academy, Changchun University of Chinese Medicine
Email: info@benthamscience.net
Kaijing Sun
Jilin Ginseng Academy, Changchun University of Chinese Medicine
Email: info@benthamscience.net
Ying Sun
, The Second Hospital of Dalian Medical University
Email: info@benthamscience.net
Wei Wu
Jilin Ginseng Academy, Changchun University of Chinese Medicine
Email: info@benthamscience.net
Changbao Chen
Jilin Ginseng Academy, Changchun University of Chinese Medicine
Email: info@benthamscience.net
Xin Jin
Key Laboratory of Molecular Epigenetics of the Ministry of Education (MOE), Northeast Normal University
Autor responsável pela correspondência
Email: info@benthamscience.net
Xilin Wan
Jilin Ginseng Academy, Changchun University of Chinese Medicine
Autor responsável pela correspondência
Email: info@benthamscience.net
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