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Mst1 regulates non-small cell lung cancer A549 cell apoptosis by inducing mitochondrial damage via ROCK1/F‑actin

Weiqiang Zhang1, Keiqiang Liu1, Yingxin Pei1

  • 1Department of Thoracic Surgery, Army General Hospital of PLA, Beijing 100700, P.R. China.

International Journal of Oncology
|October 16, 2018
PubMed

Insights

Mammalian STE20-like kinase 1 (Mst1) suppresses non-small cell lung cancer (NSCLC) A549 cell growth and migration. Mst1 reintroduction activates mitochondrial apoptosis and inhibits cancer progression by modulating ROCK1/F-actin pathways.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Mammalian STE20-like kinase 1 (Mst1) is a known tumor suppressor.
  • Its specific role in non-small cell lung cancer (NSCLC) A549 cell alterations is not fully understood.
  • Mst1's involvement in mitochondrial homeostasis and ROCK1/F-actin pathways requires further investigation.

Purpose of the Study:

  • To investigate the functional role of Mst1 in NSCLC A549 cell proliferation, migration, and apoptosis.
  • To elucidate the underlying molecular mechanisms involving mitochondrial homeostasis and ROCK1/F-actin pathways.
  • To determine if Mst1 acts as a tumor suppressor in A549 cells.

Main Methods:

  • Mst1 expression levels were compared between A549 cells and normal pulmonary epithelial cells.
  • Mst1 was overexpressed in A549 cells to assess its effects on cell viability, apoptosis, proliferation, and migration.
  • Mitochondrial function, including potential, ROS production, and cytochrome c release, was analyzed.
  • ROCK1/F-actin pathways were inhibited to observe effects on mitochondrial homeostasis and apoptosis.
  • Caspase-9-dependent apoptosis was evaluated.

Main Results:

  • Mst1 expression was significantly downregulated in A549 cells compared to normal cells.
  • Mst1 overexpression reduced A549 cell viability, promoted apoptosis, and suppressed proliferation and migration.
  • Mst1 reintroduction activated mitochondrial apoptosis pathways, evidenced by decreased mitochondrial potential, increased ROS, and cytochrome c release.
  • Mst1 overexpression impaired mitochondrial respiratory function and suppressed cellular energy metabolism.
  • Mst1 activated ROCK1/F-actin pathways, crucial for mitochondrial function regulation.
  • Inhibition of ROCK1/F-actin pathways reversed Mst1's effects, preserving mitochondrial homeostasis and promoting cell survival.

Conclusions:

  • Mst1 acts as a tumor suppressor in NSCLC A549 cells.
  • Mst1 regulates A549 cell survival through the ROCK1/F-actin pathway, impacting mitochondrial homeostasis and apoptosis.
  • These findings suggest Mst1 as a potential therapeutic target for NSCLC treatment.

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