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Salinomycin suppresses TGF-β1-induced EMT by down-regulating MMP-2 and MMP-9 via the AMPK/SIRT1 pathway in non-small

Ki-Eun Hwang1, Hyo-Jin Kim2, In-Sol Song1

  • 1Department of Internal Medicine, Wonkwang University, School of Medicine, Iksan, Jeonbuk 54538, Republic of Korea.

International Journal of Medical Sciences
|January 13, 2021
PubMed

Insights

Salinomycin (Sal) inhibits non-small cell lung cancer (NSCLC) cell migration and invasion by blocking TGF-β1-induced epithelial-to-mesenchymal transition (EMT). It targets MMP-2 and MMP-9 via the AMPK/SIRT pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Non-small cell lung cancer (NSCLC) cell migration and invasion are critical for metastasis.
  • Transforming growth factor-β1 (TGF-β1) is a key inducer of epithelial-to-mesenchymal transition (EMT), promoting cancer cell motility.
  • The anti-tumor drug Salinomycin (Sal) has shown potential, but its specific effects on NSCLC cell migration and invasion are not fully understood.

Purpose of the Study:

  • To investigate the inhibitory effects of Salinomycin on TGF-β1-induced EMT and cell migration in NSCLC.
  • To elucidate the underlying molecular mechanisms, including the roles of AMPK/SIRT signaling and matrix metalloproteinases (MMPs).

Main Methods:

  • Investigated Sal's effects on TGF-β1-induced EMT markers (E-cadherin, mesenchymal markers).
  • Assessed Sal's impact on AMPK/SIRT signaling pathway activity.
  • Examined the role of MMP-2 and MMP-9 in Sal's inhibitory effects using knockdown and activator treatments.
  • Utilized pharmacological inhibition and gene knockdown of AMPK and SIRT1.

Main Results:

  • Salinomycin effectively blocked TGF-β1-induced cell migration and invasion by reversing EMT.
  • Sal restored E-cadherin expression and suppressed mesenchymal markers.
  • Sal inhibited TGF-β1-mediated upregulation of AMPK/SIRT signaling and downstream MMP-2/MMP-9.
  • Knockdown of AMPK, SIRT1, MMP-2, or MMP-9 synergized with Sal to inhibit TGF-β1-induced EMT and invasion.

Conclusions:

  • Salinomycin suppresses TGF-β1-induced EMT, migration, and invasion in NSCLC cells.
  • This suppression is mediated by downregulating MMP-2 and MMP-9 through the AMPK/SIRT pathway.
  • Salinomycin represents a potential therapeutic agent for inhibiting NSCLC progression.
Keywords:
AMPKEMTLung cancerMMPSIRTSalinomycinTGF-β1

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