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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

Published on: April 21, 2022

Malignant pleural mesothelioma cells resist anoikis as quiescent pluricellular aggregates

J Daubriac1, J Fleury-Feith, L Kheuang

  • 1INSERM, U674, Fondation Jean Dausset-CEPH, IFR105, Paris, France.

Cell Death and Differentiation
|April 4, 2009
PubMed

Insights

Malignant pleural mesothelioma cells resist anoikis by forming aggregates, unlike normal cells. Intercellular contact is crucial for this survival, highlighting a key difference in cancer cell behavior.

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Pleural fluid accumulation is common in malignant pleural mesothelioma (MPM).
  • Free spheroid aggregates of malignant cells in pleural fluid raise questions about anoikis resistance.
  • Understanding MPM cell survival mechanisms is critical for treatment.

Purpose of the Study:

  • To investigate the mechanisms of anoikis resistance in malignant pleural mesothelioma cells.
  • To compare the behavior of MPM cells and non-tumoral mesothelial cells under non-adherent conditions.
  • To identify signaling pathways involved in MPM cell survival and anoikis.

Main Methods:

  • Culturing MPM cells and non-tumoral mesothelial cells under non-adherent conditions.
  • Analyzing cell viability, aggregate formation, and cell cycle progression.
  • Investigating the role of PI3K/Akt, ERK, and SAPK/JNK signaling pathways.
  • Utilizing anisomycin to activate SAPK/JNK and examining Bim and caspase-9 involvement.

Main Results:

  • MPM cells form viable, organized aggregates under non-adherent conditions, entering G(0).
  • Loss of anchorage inactivates PI3K/Akt, ERK, and SAPK/JNK pathways in MPM cells.
  • Non-tumoral mesothelial cells undergo anoikis via SAPK/JNK, Bim, and caspase-9.
  • Activating SAPK/JNK with anisomycin reverses MPM cell survival via a Bim-dependent mitochondrial pathway.
  • Impaired cell aggregation in MPM cells activates SAPK/JNK and Bim, inducing anoikis.

Conclusions:

  • Intercellular contacts are essential for anoikis resistance in malignant pleural mesothelioma cells.
  • MPM cells exhibit unique survival mechanisms compared to non-tumoral mesothelial cells.
  • Targeting intercellular communication or specific pathways may offer therapeutic strategies for MPM.

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