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20 (S)-ginsenoside Rh2 inhibits colorectal cancer cell growth by suppressing the Axl signaling pathway in vitro and in vivo

Title
20 (S)-ginsenoside Rh2 inhibits colorectal cancer cell growth by suppressing the Axl signaling pathway in vitro and in vivo
Authors
Zhang, HaiboYi, Jun KooHuang, HaiPark, SijunKwon, WookbongKim, EungyungJang, SoyoungKim, Si YongChoi, Seong-KyoonYoon, DuhakKim, Sung HyunLiu, KangdongDong, ZigangRyoo, Zae YoungKim, Myoung Ok
DGIST Authors
Zhang, Haibo; Yi, Jun Koo; Huang, Hai; Park, Sijun; Kwon, Wookbong; Kim, Eungyung; Jang, Soyoung; Kim, Si Yong; Choi, Seong-Kyoon; Yoon, Duhak; Kim, Sung Hyun; Liu, Kangdong; Dong, Zigang; Ryoo, Zae Young; Kim, Myoung Ok
Issue Date
2022-05
Citation
Journal of Ginseng Research, 46(3), 396-407
Type
Article
Author Keywords
Colorectal cancerXenograft20(S)-ginsenoside Rh2Axl
Keywords
RECEPTOR TYROSINE KINASEEGFR-TKIRESISTANCEPI3K/AKTSURVIVALERK1/2SRCPROLIFERATIONCHEMOTHERAPYACTIVATION
ISSN
1226-8453
Abstract
Background: Colorectal cancer (CRC) has a high morbidity and mortality worldwide. 20 (S)-ginsenoside Rh2 (G-Rh2) is a natural compound extracted from ginseng, which exhibits anticancer effects in many cancer types. In this study, we demonstrated the effect and underlying molecular mechanism of G-Rh2 in CRC cells in vitro and in vivo. Methods: Cell proliferation, migration, invasion, apoptosis, cell cycle, and western blot assays were performed to evaluate the effect of G-Rh2 on CRC cells. In vitro pull-down assay was used to verify the interaction between G-Rh2 and Axl. Transfection and infection experiments were used to explore the function of Axl in CRC cells. CRC xenograft models were used to further investigate the effect of Axl knockdown and G-Rh2 on tumor growth in vivo. Results: G-Rh2 significantly inhibited proliferation, migration, and invasion, and induced apoptosis and G0/G1 phase cell cycle arrest in CRC cell lines. G-Rh2 directly binds to Axl and inhibits the Axl signaling pathway in CRC cells. Knockdown of Axl suppressed the growth, migration and invasion ability of CRC cells in vitro and xenograft tumor growth in vivo, whereas overexpression of Axl promoted the growth, migration, and invasion ability of CRC cells. Moreover, G-Rh2 significantly suppressed CRC xenograft tumor growth by inhibiting Axl signaling with no obvious toxicity to nude mice. Conclusion: Our results indicate that G-Rh2 exerts anticancer activity in vitro and in vivo by suppressing the Axl signaling pathway. G-Rh2 is a promising candidate for CRC prevention and treatment. © 2021
URI
http://hdl.handle.net/20.500.11750/15617
DOI
10.1016/j.jgr.2021.07.004
Publisher
Elsevier BV
Related Researcher
Files:
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Collection:
Division of Biotechnology1. Journal Articles


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