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Article

Changes in the Expression of Genes Regulating the Response to Hypoxia, Inflammation, Cell Cycle, Apoptosis, and Epithelial Barrier Functioning during Colitis-Associated Colorectal Cancer Depend on Individual Hypoxia Tolerance

1
Avtsyn Research Institute of Human Morphology of Federal State Budgetary Scientific Institution “Petrovsky National Research Centre of Surgery”, 117418 Moscow, Russia
2
Research Institute of Molecular and Cellular Medicine, People’s Friendship University of Russia (RUDN University), 117198 Moscow, Russia
3
National Medical Research Center for Obstetrics, Gynecology and Perinatology Named after Academician V.I. Kulakov of Ministry of Health of Russian Federation, 117513 Moscow, Russia
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2024, 25(14), 7801; https://doi.org/10.3390/ijms25147801 (registering DOI)
Submission received: 13 June 2024 / Revised: 2 July 2024 / Accepted: 8 July 2024 / Published: 16 July 2024

Abstract

One of the factors contributing to colorectal cancer (CRC) development is inflammation, which is mostly hypoxia-associated. This study aimed to characterize the morphological and molecular biological features of colon tumors in mice that were tolerant and susceptible to hypoxia based on colitis-associated CRC (CAC). Hypoxia tolerance was assessed through a gasping time evaluation in a decompression chamber. One month later, the animals were experimentally modeled for colitis-associated CRC by intraperitoneal azoxymethane administration and three dextran sulfate sodium consumption cycles. The incidence of tumor development in the distal colon in the susceptible to hypoxia mice was two times higher and all tumors (100%) were represented by adenocarcinomas, while in the tolerant mice, only 14% were adenocarcinomas and 86% were glandular intraepithelial neoplasia. The tumor area assessed on serially stepped sections was statistically significantly higher in the susceptible animals. The number of macrophages, CD3−CD19+, CD3+CD4+, and NK cells in tumors did not differ between animals; however, the number of CD3+CD8+ and vimentin+ cells was higher in the susceptible mice. Changes in the expression of genes regulating the response to hypoxia, inflammation, cell cycle, apoptosis, and epithelial barrier functioning in tumors and the peritumoral area depended on the initial mouse’s hypoxia tolerance, which should be taken into account for new CAC diagnostics and treatment approaches development.
Keywords: colitis-associated colorectal cancer; inflammation; immunity cells; cytokines; hypoxia tolerance; gene expression colitis-associated colorectal cancer; inflammation; immunity cells; cytokines; hypoxia tolerance; gene expression

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MDPI and ACS Style

Dzhalilova, D.; Silina, M.; Tsvetkov, I.; Kosyreva, A.; Zolotova, N.; Gantsova, E.; Kirillov, V.; Fokichev, N.; Makarova, O. Changes in the Expression of Genes Regulating the Response to Hypoxia, Inflammation, Cell Cycle, Apoptosis, and Epithelial Barrier Functioning during Colitis-Associated Colorectal Cancer Depend on Individual Hypoxia Tolerance. Int. J. Mol. Sci. 2024, 25, 7801. https://doi.org/10.3390/ijms25147801

AMA Style

Dzhalilova D, Silina M, Tsvetkov I, Kosyreva A, Zolotova N, Gantsova E, Kirillov V, Fokichev N, Makarova O. Changes in the Expression of Genes Regulating the Response to Hypoxia, Inflammation, Cell Cycle, Apoptosis, and Epithelial Barrier Functioning during Colitis-Associated Colorectal Cancer Depend on Individual Hypoxia Tolerance. International Journal of Molecular Sciences. 2024; 25(14):7801. https://doi.org/10.3390/ijms25147801

Chicago/Turabian Style

Dzhalilova, Dzhuliia, Maria Silina, Ivan Tsvetkov, Anna Kosyreva, Natalia Zolotova, Elena Gantsova, Vladimir Kirillov, Nikolay Fokichev, and Olga Makarova. 2024. "Changes in the Expression of Genes Regulating the Response to Hypoxia, Inflammation, Cell Cycle, Apoptosis, and Epithelial Barrier Functioning during Colitis-Associated Colorectal Cancer Depend on Individual Hypoxia Tolerance" International Journal of Molecular Sciences 25, no. 14: 7801. https://doi.org/10.3390/ijms25147801

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