AI Article Synopsis
- Deletion of PRMT5 in mouse gastric epithelium leads to spontaneous intestinal-type gastric cancer, with some cases progressing to invasive cancer by 8 months.
- PRMT5 loss is linked to an increase in Lgr5 stem cells, which contribute to gastric tumorigenesis and activate Wnt/β-catenin signaling, a key driver of tumor development.
- In human gastric cancer samples, PRMT5 deletion and downregulation correlate with poor prognosis, suggesting it acts as a tumor suppressor in gastric tumor formation.
Article Abstract
Previous studies have demonstrated the oncogenic role of protein arginine methyltransferase 5 (PRMT5) in gastric cancer cell lines. The function of PRMT5 in gastric tumorigenesis, however, is still unexplored. Here, we showed that deletion in mouse gastric epithelium resulted in spontaneous tumorigenesis in gastric antrum. All -deficient mice displayed intestinal-type gastric cancer within 4 months of age. Of note, 20% (2/10) of mutants finally developed into invasive gastric cancer by 8 months of age. Gastric cancer caused by PRMT5 loss exhibited the increase in Lgr5 stem cells, which are proposed to contribute to both the gastric tumorigenesis and progression in mouse models. Consistent with the notion that Lgr5 is the target of Wnt/β-catenin signaling, whose activation is the most predominant driver for gastric tumorigenesis, mutant gastric cancer showed the activation of Wnt/β-Catenin signaling. Furthermore, in human gastric cancer samples, deletion and downregulation were frequently observed and associated with the poor prognosis. We propose that as opposed to the tumor-promoting role of PRMT5 well-established in the progression of various cancer types, PRMT5 functions as a tumor suppressor , at least during gastric tumor formation.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9295066 | PMC |
| http://dx.doi.org/10.7150/ijbs.71581 | DOI Listing |
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