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Updated: Jun 29, 2025

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Suppression of JAK2/STAT3 Pathway by Notoginsenoside R1 Reduces Epithelial-Mesenchymal Transition in Non-small Cell

Min Wan1, Hong Yu1, Haoqing Zhai2

  • 1Department of Medical Laboratory, Wuhan Hospital of Traditional Chinese Medicine, Wuhan, 430014, China.

Molecular Biotechnology
|April 2, 2024
PubMed

Insights

Notoginsenoside R1 (NGR1) effectively inhibits non-small cell lung cancer (NSCLC) growth and metastasis. NGR1 restrains the epithelial-mesenchymal transition (EMT) process by inactivating the JAK2/STAT3 signaling pathway, showing therapeutic potential for NSCLC.

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Non-small cell lung cancer (NSCLC) remains a leading cause of cancer mortality worldwide.
  • Novel therapeutic agents targeting NSCLC progression are urgently needed.
  • Notoginsenoside R1 (NGR1), a saponin, has demonstrated potential anti-tumor activities.

Purpose of the Study:

  • To investigate the anti-cancer role and underlying mechanism of NGR1 in non-small cell lung cancer (NSCLC).
  • To evaluate the effect of NGR1 on NSCLC cell viability, proliferation, migration, and invasiveness.
  • To elucidate the impact of NGR1 on epithelial-mesenchymal transition (EMT) and the JAK2/STAT3 pathway in NSCLC.

Main Methods:

  • Ex vivo assays were used to assess NSCLC cell behavior (viability, proliferation, migration, invasiveness).
  • NSCLC xenograft mouse models were established for in vivo validation.
  • Immunoblotting and immunohistochemistry analyzed EMT markers and JAK2/STAT3 pathway proteins.

Main Results:

  • NGR1 significantly suppressed NSCLC cell growth both ex vivo and in vivo.
  • NGR1 reduced the migratory and invasive potential of NSCLC cells.
  • NGR1 inhibited EMT by increasing E-cadherin and decreasing N-cadherin, vimentin, and snail expression, while also inactivating the JAK2/STAT3 pathway.

Conclusions:

  • NGR1 exhibits potent anti-NSCLC effects by restraining the epithelial-mesenchymal transition (EMT) process.
  • The mechanism involves the inactivation of the JAK2/STAT3 signaling pathway.
  • NGR1 represents a promising therapeutic candidate for non-small cell lung cancer treatment.
Keywords:
EMTMetastasisNon-small cell lung cancerNotoginsenoside R1

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