AI Article Synopsis
- Colorectal cancer is a major global health issue, with emerging research highlighting the role of certain infections in its development, spread, and resistance to treatment.
- The study demonstrates that the infection leads to increased expression of ANGPTL4, which in turn enhances glucose uptake and glycolysis in colorectal cancer cells, facilitating the infection's colonization.
- Additionally, the research reveals that the elevated acetylation of histone H3 lysine 27 in infected cancer cells contributes to the upregulation of ANGPTL4, suggesting potential new therapeutic targets to combat infection-related colorectal cancer progression.
Article Abstract
Colorectal cancer is a severe health problem worldwide, and accumulating evidence supports the contribution of () to colorectal cancer development, metastasis, and chemoresistance. However, the mechanisms underlying the colonization of in colorectal cancer tissue are not yet clarified. Here we demonstrate that infection mediated elevation of angiopoietin-like 4 (ANGPTL4) expression. Upregulated ANGPTL4 promoted glucose uptake and glycolysis activity in colorectal cancer cells and , which are necessary for the colonization of . Furthermore, overall increased acetylation of histone H3 lysine 27 was observed in -infected colorectal cancer cells and patient tumors, which was responsible for the corresponding transcriptional upregulation of ANGPTL4. These data indicate that the metabolic reprogramming of cancer cells induced by is essential for its enrichment and persistence in colorectal cancer, providing a novel potential target for the clinical intervention of -related colorectal cancer. SIGNIFICANCE: colonization in colorectal cancer is regulated by ANGPTL4-mediated glycolysis, suggesting that this axis could be targeted for combined repression of and cancer progression.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9397643 | PMC |
| http://dx.doi.org/10.1158/0008-5472.CAN-21-2273 | DOI Listing |
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