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Ginsenoside Rh3 Inhibits Lung Cancer Metastasis by Targeting Extracellular Signal-Regulated Kinase: A Network
Xiaodan Xue1,2,3, Yannan Liu1,2,3, Linlin Qu1,2,3
1Shaanxi Key Laboratory of Degradable Biomedical Materials, School of Chemical Engineering, Northwest University, Taibai North Road 229, Xi'an 710069, China.
Abstract:
Lung cancer has a high mortality rate and is very common. One of the main reasons for the poor prognosis of patients with lung cancer is the high incidence of metastasis. Ginsenoside Rh3, a rare ginsenoside extracted from Panax notoginseng, exhibits excellent anti-inflammatory and anti-tumor effects. Nonetheless, the inhibitory potential of Rh3 against lung cancer remains unknown. The target genes of Rh3 were screened by the PharmMapper database; the proliferation of lung cancer cells was detected by MTT assay; the migration and invasion of cells were detected by the Transwell method; and the expression of extracellular signal-regulated kinase (ERK) and EMT-related proteins in vivo and in vitro were detected by Western blotting. In addition, we established a lung metastasis model in nude mice using A549 cells to assess the effect of Rh3 on NSCLC tumor metastasis in vivo. Our findings suggest that Rh3 significantly inhibited lung cancer metastasis both in vivo and in vitro. It was determined by flow cytometry analysis that Rh3 notably inhibited cell proliferation by blocking the G1 phase. In addition, Rh3 inhibited metastasis in lung cancer cells and regulated the expression of metastasis-related proteins under hypoxia. Mechanistic studies suggested that Rh3 targeted ERK to inhibit lung cancer metastasis. The ERK inhibitor U0126 or siRNA-mediated knockdown of ERK had an enhanced effect on Rh3's ability to inhibit lung cancer metastasis. The studies revealed that the inhibitory effect of Rh3 on the metastatic ability of lung cancer cells may be supported by ERK-related signaling pathways.
Insights
Ginsenoside Rh3 effectively inhibits lung cancer metastasis and proliferation by targeting the ERK pathway. This natural compound shows promise in reducing non-small cell lung cancer (NSCLC) spread and growth.
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Lung cancer exhibits high mortality and metastasis is a primary cause of poor patient prognosis.
- Ginsenoside Rh3, derived from Panax notoginseng, possesses known anti-inflammatory and anti-tumor properties.
- The anti-metastatic potential of Ginsenoside Rh3 in lung cancer was previously unexplored.
Purpose of the Study:
- To investigate the inhibitory effects of Ginsenoside Rh3 on lung cancer metastasis and proliferation.
- To elucidate the molecular mechanisms underlying Ginsenoside Rh3's anti-cancer activity, focusing on the ERK pathway.
- To evaluate the efficacy of Ginsenoside Rh3 in preclinical models of lung cancer metastasis.
Main Methods:
- Screening of Ginsenoside Rh3 target genes using the PharmMapper database.
- In vitro assessment of lung cancer cell proliferation (MTT assay), migration, and invasion (Transwell assay).
- In vivo evaluation using a nude mouse model of lung metastasis and Western blotting for protein expression analysis (ERK and EMT markers).
Main Results:
- Ginsenoside Rh3 significantly inhibited lung cancer cell proliferation by arresting cells in the G1 phase.
- In vitro and in vivo studies demonstrated that Ginsenoside Rh3 effectively suppressed lung cancer metastasis.
- Mechanistic studies revealed that Ginsenoside Rh3 targets the extracellular signal-regulated kinase (ERK) pathway to inhibit metastasis, an effect potentiated by ERK inhibition.
Conclusions:
- Ginsenoside Rh3 exhibits significant anti-metastatic and anti-proliferative effects against lung cancer.
- The anti-metastatic action of Ginsenoside Rh3 is mediated through the regulation of the ERK signaling pathway.
- Ginsenoside Rh3 represents a potential therapeutic agent for combating lung cancer metastasis.
