Inflammasomes Are Influenced by Epigenetic and Autophagy Mechanisms in Colorectal Cancer Signaling.

Int J Mol Sci

Immunology Division, Department of Internal Medicine and Hematology, Semmelweis University, 1088 Budapest, Hungary.

Published: June 2024

AI Article Synopsis

  • Inflammasomes play a key role in promoting inflammation within the tumor microenvironment of colorectal cancer (CRC), which can enhance tumor growth and cause tissue damage.
  • The regulation of inflammasomes is influenced by epigenetic processes, offering potential new targets for therapeutic interventions in CRC.
  • The interplay between inflammasomes, autophagy, and epigenetic changes creates a complex network that researchers are exploring for new treatments for colorectal cancer.

Article Abstract

Inflammasomes contribute to colorectal cancer signaling by primarily inducing inflammation in the surrounding tumor microenvironment. Its role in inflammation is receiving increasing attention, as inflammation has a protumor effect in addition to inducing tissue damage. The inflammasome's function is complex and controlled by several layers of regulation. Epigenetic processes impact the functioning or manifestation of genes that are involved in the control of inflammasomes or the subsequent signaling cascades. Researchers have intensively studied the significance of epigenetic mechanisms in regulation, as they encompass several potential therapeutic targets. The regulatory interactions between the inflammasome and autophagy are intricate, exhibiting both advantageous and harmful consequences. The regulatory aspects between the two entities also encompass several therapeutic targets. The relationship between the activation of the inflammasome, autophagy, and epigenetic alterations in CRC is complex and involves several interrelated pathways. This article provides a brief summary of the newest studies on how epigenetics and autophagy control the inflammasome, with a special focus on their role in colorectal cancer. Based on the latest findings, we also provide an overview of the latest therapeutic ideas for this complex network.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11173330PMC
http://dx.doi.org/10.3390/ijms25116167DOI Listing

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