20 (S)-ginsenoside Rh2 inhibits colorectal cancer cell growth by suppressing the Axl signaling pathway in vitro and in vivo
Keywords
- Panax
- Western blotting
- antineoplastic activity
- apoptosis
- cell cycle checkpoints
- cell growth
- cell proliferation
- colorectal neoplasms
- morbidity
- mortality
- neoplasm cells
- research
- toxicity
- transfection
- xenotransplantation
- 20(S)-ginsenoside Rh2
- Axl
- Colorectal cancer
- Xenograft
Publication Dbxref
AGL:7529251
Title
20 (S)-ginsenoside Rh2 inhibits colorectal cancer cell growth by suppressing the Axl signaling pathway in vitro and in vivo
Publication Type
Journal Article
Series Name
Journal of Ginseng Research
Volume
46
Publication Year
2022
Issue
3
Page Numbers
396-407
Publication Date
2022
Citation
Zhang H, Yi J, Huang H, Park S, Kwon W, Kim E, Jang S, Kim S, Choi S, Yoon D, Kim S, Liu K, Dong Z, Ryoo ZY, Kim MO. 20 (S)-ginsenoside Rh2 inhibits colorectal cancer cell growth by suppressing the Axl signaling pathway in vitro and in vivo. Journal of Ginseng Research. 2022; 46(3):396-407.
Language Abbr
eng
Abstract
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. 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. 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. 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.
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