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A Modified In vitro Invasion Assay to Determine the Potential Role of Hormones, Cytokines and/or Growth Factors in Mediating Cancer Cell Invasion
06:36

A Modified In vitro Invasion Assay to Determine the Potential Role of Hormones, Cytokines and/or Growth Factors in Mediating Cancer Cell Invasion

Published on: April 24, 2015

Non-small cell lung cancer cyclooxygenase-2-dependent invasion is mediated by CD44

M Dohadwala1, J Luo, L Zhu

  • 1Lung Cancer Research Program of the UCLA Jonsson Comprehensive Cancer Center, Division of Pulmonary Medicine, Department of Medicine, UCLA, School of Medicine, Los Angeles California 90095-1690, USA.

The Journal of Biological Chemistry
|April 26, 2001
PubMed

Insights

Cyclooxygenase-2 (COX-2) promotes non-small cell lung cancer (NSCLC) invasion via CD44. Inhibiting COX-2 may offer a therapeutic strategy for NSCLC by reducing tumor invasiveness.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Elevated cyclooxygenase-2 (COX-2) expression in tumors correlates with increased angiogenesis, invasion, and immune suppression.
  • Previous research demonstrated that genetic inhibition of COX-2 reverses non-small cell lung cancer (NSCLC)-induced immunosuppression.

Purpose of the Study:

  • To investigate the role of COX-2 expression in lung cancer invasiveness.
  • To elucidate the molecular mechanisms underlying COX-2-mediated tumor invasion in NSCLC.

Main Methods:

  • Non-small cell lung cancer (NSCLC) cell lines were genetically modified using retroviral vectors to express human COX-2 cDNA in sense (COX-2-S) and antisense (COX-2-AS) orientations.
  • Assessed COX-2 protein levels, prostaglandin E(2) production, and invasive capacity of modified cell lines.
  • Investigated the role of CD44, a cell surface receptor, in COX-2-mediated invasion through specific blockade experiments.

Main Results:

  • COX-2-S clones exhibited significantly higher COX-2 protein expression and prostaglandin E(2) production compared to controls.
  • COX-2-S cells demonstrated enhanced invasive capacity, which was significantly reduced by CD44 blockade.
  • COX-2-AS clones showed limited invasion and diminished CD44 expression.

Conclusions:

  • A COX-2-mediated, CD44-dependent pathway is implicated in non-small cell lung cancer invasion.
  • COX-2 plays a significant role in the malignant phenotype of NSCLC.
  • Targeting COX-2 could be a valuable strategy for gene or pharmacologic therapy in NSCLC treatment.

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