The microbiota and aging microenvironment in pancreatic cancer: Cell origin and fate

Cellular senescence is a state of growth arrest where nonproliferative cells accumulate over time in the aging microenvironment under multiple external factors. Senescent cells exert a double-edged sword effect in an autocrine or paracrine manner: physiologically, they contribute to tissue developme...

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Veröffentlicht in:Biochimica et biophysica acta. Reviews on cancer 2022-11, Vol.1877 (6), p.188826, Article 188826
Hauptverfasser: Chen, Zhou, Wang, Zhengfeng, Du, Yan, Shi, Huaqing, Zhou, Wence
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Sprache:eng
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Zusammenfassung:Cellular senescence is a state of growth arrest where nonproliferative cells accumulate over time in the aging microenvironment under multiple external factors. Senescent cells exert a double-edged sword effect in an autocrine or paracrine manner: physiologically, they contribute to tissue development, prevent the multiplication of damaged cells and contribute to tissue repair and tumor suppression while favoring the onset of age-related diseases, including tumors. The microbiota in human tissues is intricately linked to cellular senescence and is reportedly present in the tissues of various tumors (including pancreatic tumors), closely associated with tumorigenesis and progression. The microbiota can induce cells to undergo senescence, and their long-term effects can assist senescent cells in transforming and successfully escaping senescence, contributing to tumorigenesis and progression. Here, we focus on the correlation between the microbiota, cellular senescence, and pancreatic cancer to provide novel ideas for the study and therapy of pancreatic cancer. •Cell senescence is a double-edged sword, maintaining normal cell development and promoting tumor development.•The microbiota plays an important role in human diseases, including tumors, and can even dominate the generation and development of tumors.•Microbiota can induce cellular senescence or assist cells to circumvent cellular senescence, which has important implications in tumor generation, progression and therapy.
ISSN:0304-419X
1879-2561
DOI:10.1016/j.bbcan.2022.188826