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ORIGINAL RESEARCH article

Front. Immunol.
Sec. Cancer Immunity and Immunotherapy
Volume 15 - 2024 | doi: 10.3389/fimmu.2024.1444020
This article is part of the Research Topic Cancer Metastases: Mechanisms of Tumor Dissemination, Formation of Metastatic Niche and Anti-metastatic Therapy View all 6 articles

E-cigarette exposure disrupts antitumor immunity and promotes metastasis

Provisionally accepted
Marcel Arias Badia Marcel Arias Badia 1Chien-Chun S. Pai Chien-Chun S. Pai 1Pei Xi Chen Pei Xi Chen 1Anthony Chang Anthony Chang 1Yee May Lwin Yee May Lwin 1Aahir Srinath Aahir Srinath 1Jeffrey Gotts Jeffrey Gotts 2Stanton A. Glantz Stanton A. Glantz 1,3,4Lawrence Fong Lawrence Fong 1,4,5*
  • 1 University of California, San Francisco, San Francisco, United States
  • 2 Kaiser Permanente San Francisco Medical Center, San Francisco, California, United States
  • 3 Center for Tobacco Control Research and Education, University of California, San Francisco, San Francisco, United States
  • 4 Helen Diller Family Comprehensive Cancer Center, Medical Center, University of California, San Francisco, San Francisco, California, United States
  • 5 Parker Institute for Cancer Immunotherapy, San Francisco, California, United States

The final, formatted version of the article will be published soon.

    Electronic cigarettes (e-cigarettes) are thought to pose low risk of cancer because the components of e-cigarette liquid are not carcinogens. We analyzed the effects of the two major components, PG/VG and nicotine, on tumor development in preclinical models. We found that PG/VG promoted tumor cell migration in migration assays and contributed to more aggressive, metastatic, and immunosuppressive tumors in vivo, aggravated by the presence of nicotine. Whole body exposure of mice to PG/VG and nicotine rendered animals more susceptible to developing tumors with high frequencies of infiltrating proinflammatory macrophages expressing IL-6 and TNFα.Moreover, tumor-infiltrating and circulating T cells in e-cigarette exposed mice showed increased levels of immune checkpoints including CTLA4 and PD-1. Treatment with anti-CTLA4 antibody was able to abrogate metastasis with no detrimental effects on its ability to induce tumor regression in exposed mice. These findings suggest that the major components used in e-cigarette fluid can impact tumor development through induced immunosuppression.

    Keywords: electronic cigarettes, metastasis, whole body exposure, Immunosuppression, Immune checkpoint blockade

    Received: 04 Jun 2024; Accepted: 29 Jul 2024.

    Copyright: © 2024 Arias Badia, Pai, Chen, Chang, Lwin, Srinath, Gotts, Glantz and Fong. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Lawrence Fong, University of California, San Francisco, San Francisco, United States

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.