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Inhibition of mesothelin as a novel strategy for targeting cancer cells

Kun Wang1, Vidya Bodempudi, Zhengian Liu

  • 1Molecular Medicine Laboratory, Divisions of Gastroenterology and Hematology/Oncology, Department of Medicine, The University of Kansas Medical Center, Kansas City, Kansas, United States of America.

Plos One
|April 10, 2012
PubMed

Insights

Targeting Mesothelin, a cancer antigen, via gene silencing significantly reduced cancer cell viability and invasiveness. This approach offers a promising new strategy for developing novel cancer therapeutics against multiple malignancies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Mesothelin is a cell surface antigen implicated in various cancers, including mesothelioma, ovarian, lung, and pancreatic cancer.
  • It has been explored as a diagnostic marker and a target for immunotherapy.
  • Directly targeting Mesothelin's role in cancer cell viability is a crucial step for novel therapeutic development.

Purpose of the Study:

  • To evaluate the effects of direct Mesothelin targeting on cancer cell viability.
  • To investigate Mesothelin's role in cancer cell invasiveness and associated signaling pathways.
  • To explore the potential of Mesothelin inhibition as a therapeutic strategy for human malignancies.

Main Methods:

  • Gene-specific silencing of Mesothelin using small interfering RNA (siRNA) and microRNA (miRNA).
  • Assessment of cancer cell viability and invasiveness across various cancer cell lines (mesothelioma, ovarian, pancreatic).
  • Analysis of downstream signaling pathways including ERK1, PI3K/AKT, β-Catenin, Ero1, and cell cycle progression.

Main Results:

  • Mesothelin gene silencing significantly decreased viability and invasiveness in mesothelioma, ovarian, and pancreatic cancer cells.
  • Silencing led to reduced phospho-ERK1 and PI3K/AKT activity, and decreased β-Catenin expression, a marker of epithelial-mesenchymal transition (EMT).
  • Mesothelin inhibition also reduced Ero1 expression, induced ER-stress, and increased the fraction of cancer cells in S-phase.

Conclusions:

  • Direct inhibition of Mesothelin effectively reduces cancer cell viability and invasiveness.
  • Mesothelin silencing impacts key pro-oncogenic signaling pathways and EMT markers.
  • Targeting Mesothelin presents a potential novel therapeutic strategy for various human cancers.

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