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[Effects of MSP on Cell Cycle and EMT of Non-Small Cell Lung Cancer PC14]

Xue-Ni Shi1, Shi-Hang Wei1, Xu Peng2

  • 1College of Life Science, Sichuan University,Chengdu 610041,China.

Sichuan Da Xue Xue Bao. Yi Xue Ban = Journal of Sichuan University. Medical Science Edition
|May 9, 2018
PubMed
Abstract

Insights

Macrophage stimulating protein (MSP) halts non-small cell lung cancer cell cycle progression and inhibits epithelial-mesenchymal transition (EMT) in RON-negative PC14 cells. This suggests MSP as a potential therapeutic target for lung cancer.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Biology

Background:

  • Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related mortality.
  • Epithelial-mesenchymal transition (EMT) is a critical process in cancer progression and metastasis.
  • The role of macrophage stimulating protein (MSP) in NSCLC, particularly in RON-negative cells, requires further elucidation.

Purpose of the Study:

  • To investigate the impact of macrophage stimulating protein (MSP) on the cell cycle of non-small cell lung cancer (NSCLC) PC14 cells lacking RON expression.
  • To analyze the effect of MSP on the epithelial-mesenchymal transition (EMT) capacity of these PC14 cells.

Main Methods:

  • PC14 cells were cultured and engineered to stably express MSP (PC14-Mst1-pEGFP-N1) or a control vector (PC14-pEGFP-N1).
  • Cell cycle distribution was analyzed using flow cytometry.
  • Cellular morphology and intercellular gaps were examined via transmission electron microscopy (TEM).
  • Gene and protein expression of EMT markers (E-cadherin, Vimentin) were assessed using RT-PCR and Western blot.

Main Results:

  • MSP expression significantly increased the G1/G0 phase population while decreasing S and G2/M phases in PC14 cells.
  • Intercellular gaps between PC14-Mst1-pEGFP-N1 cells were reduced compared to controls.
  • RT-PCR and Western blot revealed significantly elevated E-cadherin and reduced Vimentin mRNA and protein levels in MSP-expressing cells.

Conclusions:

  • Macrophage stimulating protein (MSP) influences the cell cycle of RON-negative PC14 cells, promoting G1/G0 arrest.
  • MSP inhibits the epithelial-mesenchymal transition (EMT) in these cells by upregulating E-cadherin and downregulating Vimentin.
  • These findings suggest MSP's potential as a therapeutic target for NSCLC, particularly in tumors lacking RON expression.
Keywords:
Cell cycleEpithelial mesenchymal transitionMacrophage stimulating proteinPC14 cell

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