Multifaceted MRVI1 Serves as a Tumor Suppressor in HCT116 Colorectal Cancer Cells.
1/5 보강
MRVI1 is a multifaceted gene whose functions in cancer vary across tissue types, acting either as a tumor-promoting or tumor-suppressive factor.
APA
Higashi K, Cho Y, Aoyama K (2026). Multifaceted MRVI1 Serves as a Tumor Suppressor in HCT116 Colorectal Cancer Cells.. Biological & pharmaceutical bulletin, 49(3), 589-593. https://doi.org/10.1248/bpb.b25-00756
MLA
Higashi K, et al.. "Multifaceted MRVI1 Serves as a Tumor Suppressor in HCT116 Colorectal Cancer Cells.." Biological & pharmaceutical bulletin, vol. 49, no. 3, 2026, pp. 589-593.
PMID
41905951 ↗
Abstract 한글 요약
MRVI1 is a multifaceted gene whose functions in cancer vary across tissue types, acting either as a tumor-promoting or tumor-suppressive factor. In colorectal cancer, MRVI1 functions downstream of p53, and its loss enhances malignant phenotypes; however, the effects of MRVI1 overexpression have remained unclear. In this study, we established HCT116 colorectal cancer cells stably overexpressing MRVI1 to examine its functional impact. Western blot analysis confirmed robust expression of the V5-TurboID-MRVI1 fusion protein in the established cell line. Cell proliferation assays showed that MRVI1 overexpression markedly reduced cell growth compared with control cells under standard culture conditions. Trypan blue staining demonstrated that MRVI1 overexpression did not increase cell death, indicating that the reduction in cell number reflects a cytostatic rather than cytotoxic effect. These findings provide direct evidence that MRVI1 suppresses the proliferation of colorectal cancer cells when overexpressed. Combined with previous reports demonstrating that MRVI1 knockdown promotes proliferation and invasive behavior in colorectal cancer cells, our results support the view that MRVI1 contributes to p53-associated growth control in this tumor lineage. These observations further reinforce the concept that MRVI1 is a context-dependent, multifaceted cancer-associated gene.
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