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精氨酸甲基转移酶 PRMT3 通过调节结直肠癌中 c-MYC 的稳定促进肿瘤发生。

Arginine methyltransferase PRMT3 promote tumorigenesis through regulating c-MYC stabilization in colorectal cancer.

机构信息

Department of General Surgery, Xiantao First People's Hospital Affiliated to Yangtze University, Xiantao, Hubei, China.

Department of General Surgery, Xiantao First People's Hospital Affiliated to Yangtze University, Xiantao, Hubei, China.

出版信息

Gene. 2021 Jul 30;791:145718. doi: 10.1016/j.gene.2021.145718. Epub 2021 May 13.

Abstract

The incidence rates of colorectal cancer have been increasing in the last decades, yet the overall survival rate is still not ideal. There is a need to further investigate detailed mechanism for colorectal cancer tumorigenesis. The biological function of protein arginine methyltransferases 3 (PRMT3) is seldom studied in tumorigenesis. Here, we attempted to elucidate the link between PRMT3 and tumorigenesis in colorectal cancer. Results revealed that PRMT3 was upregulated in colorectal cancer. Besides, PRMT3 overexpression promoted colorectal cancer cell proliferation, migration, and invasion. Regarding mechanism for colorectal cancer tumorigenesis, PRMT3 stabilized C-MYC and the pro-tumorigenesis function of PRMT3 was dependent on C-MYC. Clinically, these findings might provide a novel therapeutical treatment strategy for colorectal cancer.

摘要

在过去几十年中,结直肠癌的发病率一直在上升,但总体生存率仍然不理想。需要进一步研究结直肠癌发生的详细机制。在肿瘤发生中,蛋白质精氨酸甲基转移酶 3(PRMT3)的生物学功能很少被研究。在这里,我们试图阐明 PRMT3 与结直肠癌发生之间的联系。结果表明,PRMT3 在结直肠癌中上调。此外,PRMT3 的过表达促进了结直肠癌细胞的增殖、迁移和侵袭。关于结直肠癌发生的机制,PRMT3 稳定了 C-MYC,PRMT3 的促肿瘤发生功能依赖于 C-MYC。临床上,这些发现可能为结直肠癌提供新的治疗策略。

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