Gypenosides Damulin A and Damulin B Inhibit Hepatocellular Carcinoma by Regulating Cholesterol Synthesis.

Authors

Fang-Fang Li, Can Cui, Zhou-Juan Zheng, Man-Yu Xiao, Si Li, Peng Xie, Xiang-Lan Piao

Published in

Drug development research. Volume 87. Issue 7. Pages e70387.

Abstract

Hepatocellular carcinoma (HCC) is a common malignant tumor of the digestive system. The liver is the primary organ for cholesterol production and metabolism in the body. Abnormal cholesterol levels can promote the initiation and progression of liver cancer, as well as influence treatment and patient prognosis. Damulin A and damulin B, a pair of isomeric dammarane-type saponins isolated from heat-treated Gynostemma pentaphyllum, have been shown to inhibit HCC cell proliferation and migration, arrest the cell cycle at the G0/G1 phase, induce apoptosis, and reduce intracellular cholesterol levels in vitro. Damulin B exhibited more potent effects in these assays. RNA sequencing and Western blot analysis revealed that both compounds downregulate the expression of key cholesterol biosynthesis-related genes, namely isopentenyl-diphosphate delta isomerase 1 (IDI1) and geranylgeranyl diphosphate synthase 1 (GGPS1). However, damulin A uniquely increased the expression of other cholesterol pathway genes: farnesyl diphosphate synthase (FDPS), farnesyl-diphosphate farnesyltransferase 1 (FDFT1), and lanosterol synthase (LSS). These findings indicate that damulin A and damulin B regulate intracellular cholesterol biosynthesis through distinct mechanisms, which may account for their differential inhibitory effects on hepatocellular carcinoma.

PMID:
42750477
Bibliographic data and abstract were imported from PubMed on 17 Sep 2026.

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