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Ginsenoside Rg1 Suppresses Non-Small-Cell Lung Cancer via MicroRNA-126-PI3K-AKT-mTOR Pathway

Panfeng Chen1, Xiaoping Li2, Xi Yu1

  • 1Department of Respiratory and Critical Care Medicine, Tianjin First Central Hospital, Tianjin 300192, China.

Evidence-Based Complementary and Alternative Medicine : Ecam
|July 11, 2022
PubMed

Insights

Ginsenoside Rg1 inhibits non-small cell lung cancer (NSCLC) by upregulating microRNA-126 (miR-126). This pathway involves the PI3K-AKT-mTOR signaling cascade, ultimately promoting apoptosis and reducing cancer cell viability.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Lung cancer, particularly non-small cell lung cancer (NSCLC), is a leading cause of cancer mortality worldwide.
  • Ginsenoside Rg1 is recognized for its potential therapeutic roles in various diseases, including cancer.
  • MicroRNA-126 (miR-126) is implicated in the pathogenesis of several cancers, with its expression often altered in tumor tissues.

Purpose of the Study:

  • To investigate the anti-cancer effects of Ginsenoside Rg1 on NSCLC.
  • To elucidate the underlying molecular mechanisms, focusing on the role of miR-126.

Main Methods:

  • Utilized NSCLC cell lines (A549, H1650) and patient samples (PBMC, tumor, and paracancerous tissues).
  • Assessed the impact of Ginsenoside Rg1 and miR-126 knockdown (KD) on cell viability and apoptosis.
  • Employed bioinformatics analysis and Western blot (WB) assays to investigate the miR-126 targeting of the PI3K signaling pathway, including PI3KR2 and mTOR.

Main Results:

  • miR-126 expression was significantly decreased in NSCLC patients' PBMCs and tumor tissues compared to controls.
  • Ginsenoside Rg1 inhibited NSCLC cell growth and proliferation.
  • miR-126 KD increased apoptosis gene expression (caspase 3, caspase 9) and decreased cell viability.
  • miR-126 was confirmed to target the PI3K signaling pathway, with PI3KR2 and mTOR KD affecting miR-126's pro-apoptotic function.
  • Ginsenoside Rg1's inhibitory effect on NSCLC growth was mediated through the miR-126 and mTOR pathway.

Conclusions:

  • Ginsenoside Rg1 demonstrates significant anti-NSCLC activity.
  • The mechanism involves the upregulation of miR-126, which targets the PI3K-AKT-mTOR pathway, leading to apoptosis and growth inhibition.
  • This study highlights a novel therapeutic strategy for NSCLC involving Ginsenoside Rg1 and its modulation of the miR-126 pathway.

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