The Prospective Use of 20(S)-Ginsenoside Rh2 in HCC Treatment
Introduction
Hepatocellular carcinoma (HCC) is hypervascular solid tumor with rapid deterioration, poor overall prognosis and a high recurrence rate, accounting for 90% of primary liver cancers, which has been perceived as the third most common cause of cancer-related mortality across the world. Notably, 20(S)-ginsenoside Rh2, an essential bioactive ingredient derived from ginseng, shows significant anti-tumor effects in various types of cancers, including HCC.
About HCC
There are diversified risk factors for HCC, mainly encompassing genetics, epigenetic alterations, chronic hepatitis B and C virus infections, aflatoxin exposure, smoking, obesity, and diabetes mellitus. The major therapies for HCC involve surgical excision, ablation, transcatheter arterial chemoembolization, radiotherapy, transplantation, etc. However, the overall prognosis of patients remains unsatisfactory due to the high recurrence and metastasis of HCC. Transplantation is the most effective one, yet rare matched donor livers and high surgical cost limit its application. In addition, more than 70% of advanced patients are not suitable for transplantation, either due to tumor burden or poor liver function.
The anti-angiogenetic role of ginsenoside Rh2 in HCC
Given that HCC has prominent characteristics of abnormal vascularization and angiogenesis and HCC endothelial cells are prone to forming new blood vessels in situ and supporting metastasis, targeting endothelial cell function to repress angiogenesis may be a highly promising treatment avenue for HCC.
Remarkably, 20(S)-ginsenoside Rh2 has effective anti-angiogenic activity, which can exert anti-proliferative, pro-apoptotic, and cell cycle-modulating properties in HCC cell line HepG2 by reducing VEGF and MMP-2 expressions.
Remarkably, 20(S)-ginsenoside Rh2 has effective anti-angiogenic activity, which can exert anti-proliferative, pro-apoptotic, and cell cycle-modulating properties in HCC cell line HepG2 by reducing VEGF and MMP-2 expressions.
Repressive role of 20(S)-ginsenoside Rh2 in HCC via GPC3/Wnt/β-catenin signaling
20(S)-ginsenoside Rh2 inhibits HCC growth via suppressing Wnt/β-catenin signaling pathway-related markers (β-catenin, c-myc, and cyclin D1) and GPC3, a cell-surface glycoprotein specifically overexpressed in HCC patients. Specifically, GPC3 silencing promotes 20(S)-ginsenoside Rh2-induced anti-proliferative and pro-apoptotic effects in HepG2 cells, concomitant with the downregulation of β-catenin, c-myc and cyclin D1.
Conclusion
20(S)-ginsenoside Rh2 not only inhibits angiogenesis by downregulating VEGF and MMP-2 expressions, but also targets GPC3 by downregulating the Wnt/β- catenin signaling pathway in HCC cells, opening up new opportunities for HCC treatment.
Reference
Kang I, Koo M, Jun JH, Lee J. Effect of nicotinamide mononucleotide on osteogenesis in MC3T3-E1 cells against inflammation-induced by lipopolysaccharide. Clin Exp Reprod Med. Published online April 11, 2024. doi:10.5653/cerm.2023.06744
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