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Generation and Expansion of Primary, Malignant Pleural Mesothelioma Tumor Lines
08:01

Generation and Expansion of Primary, Malignant Pleural Mesothelioma Tumor Lines

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Rat mesothelioma cell proliferation requires p38δ mitogen activated protein kinase and C/EBP-α

Jun Zhong1, Didier Lardinois, John Szilard

  • 1Pulmonary Cell Research, Department Biomedicine, University Hospital Basel, Petersgraben 4, CH-4031 Basel, Switzerland.

Lung Cancer (Amsterdam, Netherlands)
|January 14, 2011
PubMed

Insights

Platelet-derived growth factor (PDGF)-BB stimulates pleural mesothelioma cell proliferation through p38δ MAPK and C/EBP-α. Targeting these pathways may offer new therapeutic strategies for this asbestos-induced cancer.

Area of Science:

  • Oncology
  • Cell Signaling
  • Molecular Biology

Background:

  • Pleural malignant mesothelioma is a rare, asbestos-induced cancer with increasing global incidence.
  • p38 mitogen-activated protein kinases (MAPK) are implicated in mesothelioma's carcinogenesis and aggressiveness.

Purpose of the Study:

  • To investigate the roles of p38 MAPK isoforms in rat pleural mesothelioma cell proliferation.
  • To elucidate the underlying signaling pathways involved in PDGF-BB and TGF-β1 induced proliferation.

Main Methods:

  • Rat pleural mesothelioma cells were stimulated with PDGF-BB and/or TGF-β1.
  • MAPK and transcription factor activation was assessed via immunoblotting.
  • Proliferation was measured by cell count, with siRNA used to control gene expression.

Main Results:

  • PDGF-BB, not TGF-β1, induced proliferation via Erk1/2 and p38 MAPK activation.
  • p38δ MAPK translocated to the nucleus upon activation, while p38α remained in the cytosol.
  • Down-regulating Erk1/2, p38δ MAPK, or C/EBP-α suppressed PDGF-BB-induced proliferation.

Conclusions:

  • p38δ MAPK and C/EBP-α mediate proliferation in pleural mesothelioma.
  • These molecules represent potential therapeutic targets for mesothelioma treatment.

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