The Purinergic Landscape of Non-Small Cell Lung Cancer

Serena Janho Dit Hreich1, Jonathan Benzaquen1, Paul Hofman2,3,4

  • 1Institute of Research on Cancer and Aging (IRCAN, CNRS, INSERM), FHU OncoAge, Université Côte d'Azur, 06108 Nice, France.

Cancers
|April 23, 2022
PubMed

Insights

Purinergic checkpoints like CD39 and CD73 are potential targets for non-small cell lung cancer. Targeting these pathways may enhance the immune response against lung tumors.

Area of Science:

  • Oncology
  • Immunology
  • Cancer Research

Background:

  • Lung cancer remains the leading cause of cancer-related deaths globally.
  • Current treatments like targeted therapies and immune checkpoint inhibitors show limitations in managing advanced and some early-stage lung cancers.
  • Tumor progression persists in a significant proportion of lung cancer patients despite existing therapies.

Purpose of the Study:

  • To explore the role of purinergic checkpoints in the tumor immune microenvironment of non-small cell lung cancer (NSCLC).
  • To evaluate purinergic checkpoints, including CD39, CD73, P2RX7, and ADORs, as potential therapeutic targets for NSCLC.
  • To determine if targeting these checkpoints can enhance the antitumor immune response and combat NSCLC progression.

Main Methods:

  • This is a review article, thus no primary data were generated.
  • Literature search and synthesis of existing research on purinergic signaling in cancer.
  • Analysis of the function of CD39, CD73, P2RX7, and ADORs in modulating the tumor microenvironment.

Main Results:

  • Purinergic checkpoints significantly influence the immune cell composition and function within the tumor microenvironment.
  • CD39 and CD73 enzymes promote adenosine production, which suppresses antitumor immunity.
  • P2RX7 and ADORs receptors play complex roles in immune cell activation and suppression.

Conclusions:

  • Purinergic checkpoints represent promising novel therapeutic targets for non-small cell lung cancer.
  • Targeting CD39, CD73, P2RX7, and ADORs could potentially overcome resistance to current therapies.
  • Modulating purinergic signaling may enhance the efficacy of existing immunotherapies by boosting the antitumor immune response.