Unlocking the secrets: exploring the influence of the aryl hydrocarbon receptor and microbiome on cancer development.

Jochen H M Prehn, Shahab Uddin, Menatallah Rayan, Tahseen S Sayed, Ola J Hussein, Lubna Therachiyil, Zaid H Maayah, Cristina Maccalli, Hesham M Korashy

Journal: Cellular & molecular biology letters 2024;29(1):33

PMID: 38448800

Abstract

Gut microbiota regulates various aspects of human physiology by producing metabolites, metabolizing enzymes, and toxins. Many studies have linked microbiota with human health and altered microbiome configurations with the occurrence of several diseases, including cancer. Accumulating evidence suggests that the microbiome can influence the initiation and progression of several cancers. Moreover, some microbiotas of the gut and oral cavity have been reported to infect tumors, initiate metastasis, and promote the spread of cancer to distant organs, thereby influencing the clinical outcome of cancer patients. The gut microbiome has recently been reported to interact with environmental factors such as diet and exposure to environmental toxicants. Exposure to environmental pollutants such as polycyclic aromatic hydrocarbons (PAHs) induces a shift in the gut microbiome metabolic pathways, favoring a proinflammatory microenvironment. In addition, other studies have also correlated cancer incidence with exposure to PAHs. PAHs are known to induce organ carcinogenesis through activating a ligand-activated transcriptional factor termed the aryl hydrocarbon receptor (AhR), which metabolizes PAHs to highly reactive carcinogenic intermediates. However, the crosstalk between AhR and the microbiome in mediating carcinogenesis is poorly reviewed. This review aims to discuss the role of exposure to environmental pollutants and activation of AhR on microbiome-associated cancer progression and explore the underlying molecular mechanisms involved in cancer development.

© 2024. The Author(s).

Address: Department of Pharmaceutical Sciences, College of Pharmacy, QU Health, Qatar University, P. O. Box 2713, Doha, Qatar.; Department of Physiology and Medical Physics, Royal College of Surgeons in Ireland, Dublin 2, Ireland.; Department of Pharmaceutical Sciences, College of Pharmacy, QU Health, Qatar University, P. O. Box 2713, Doha, Qatar.; Department of Pharmaceutical Sciences, College of Pharmacy, QU Health, Qatar University, P. O. Box 2713, Doha, Qatar.; Translational Research Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar.; Research Branch, Sidra Medicine, Doha, Qatar.; Translational Research Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar.; Dermatology Institute, Academic Health System, Hamad Medical Corporation, Doha, Qatar.; Department of Physiology and Medical Physics, Royal College of Surgeons in Ireland, Dublin 2, Ireland.; RCSI Centre for Systems Medicine, Royal College of Surgeons in Ireland, Dublin 2, Ireland.; Department of Pharmaceutical Sciences, College of Pharmacy, QU Health, Qatar University, P. O. Box 2713, Doha, Qatar. [email protected].
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