20(S)-Ginsenoside Rh2 Suppresses Oral Cancer Cell Growth by Inhibiting the Src-Raf-ERK Signaling Pathway

Related Experiment Video

Updated: Nov 22, 2025

Establishment of Hepatocarcinoma in BALB/c-nu Mice and Investigation of the Therapeutic Effect of the Sanleng Jiashen Formula
09:03

Establishment of Hepatocarcinoma in BALB/c-nu Mice and Investigation of the Therapeutic Effect of the Sanleng Jiashen Formula

Published on: January 26, 2024

562

Haibo Zhang1, Junkoo Yi2, Eungyung Kim1

  • 1Department of Animal Science and Biotechnology, Kyungpook National University, Sangju, Republic of Korea.

Anticancer Research
|January 9, 2021
PubMed
Abstract

Insights

20(S)-Ginsenoside Rh2 (G-Rh2) shows anticancer effects in oral cancer by inducing apoptosis and cell cycle arrest. This compound inhibits oral cancer cell migration and invasion, suggesting its potential as a therapeutic agent.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • 20(S)-Ginsenoside Rh2 (G-Rh2) exhibits therapeutic potential in various cancers.
  • Oral cancer remains a significant global health concern requiring novel therapeutic strategies.

Purpose of the Study:

  • To investigate the anticancer activity of G-Rh2 in oral cancer cells.
  • To elucidate the underlying molecular mechanisms of G-Rh2's action in oral cancer.

Main Methods:

  • Cell proliferation, soft agar colony formation, migration, and invasion assays were performed.
  • Cell cycle progression and apoptosis were analyzed using flow cytometry.
  • Protein expression related to epithelial-mesenchymal transition (EMT) and the Src/Raf/ERK pathway was assessed via immunoblotting.

Main Results:

  • G-Rh2 significantly inhibited oral cancer cell growth by inducing apoptosis and G0/G1-phase cell cycle arrest.
  • G-Rh2 suppressed oral cancer cell migration and invasion by modulating EMT-related proteins.
  • G-Rh2 effectively inhibited the Src/Raf/ERK signaling pathway in YD10B and Ca9-22 oral cancer cell lines.

Conclusions:

  • G-Rh2 demonstrates significant in vitro anticancer activity against oral cancer by inhibiting the Src/Raf/ERK signaling pathway.
  • G-Rh2 represents a promising therapeutic candidate for the treatment of oral cancer.
Keywords:
20(S)-Ginsenoside Rh2ERKSrcoral cancer

More Related Videos

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment11:13

Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment

Published on: June 9, 2023

1.9K
Preclinical Assessment of the Bioactivity of the Anticancer Coumarin OT48 by Spheroids, Colony Formation Assays, and Zebrafish Xenografts09:20

Preclinical Assessment of the Bioactivity of the Anticancer Coumarin OT48 by Spheroids, Colony Formation Assays, and Zebrafish Xenografts

Published on: June 26, 2018

8.7K

Related Concept Videos

The Retinoblastoma Gene01:20

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
4.4K
Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
Three regulatory proteins control their activity:
4.8K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
4.1K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
5.3K
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.9K
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a...
6.7K