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抑制 的甲基化来抑制 PC 的进展,靶向 。

inhibited the methylation of to suppress the progression of PC by targeting .

机构信息

Department of Hepatobiliary Surgery, Hainan General Hospital http://dx.doi.org/10.13039/501100001665, Haikou, P.R. China.

Department of Hepatobiliary Surgery, Hainan General Hospital http://dx.doi.org/10.13039/501100001665, Haikou, P.R. China

出版信息

Life Sci Alliance. 2023 Apr 21;6(5). doi: 10.26508/lsa.202201703. Print 2023 Apr.

Abstract

Pancreatic cancer (PC) is one of the deadliest malignancies, with poor diagnosis and prognosis. has been reported to be a tumor suppressor in various cancers, whereas the mechanism of in the progression of PC remains poorly understood. In this study, it was found that and were down-regulated, whereas was up-regulated in PC. Knockdown of or overexpression of suppressed PC cell proliferation, invasion, and migration, as well as tumor formation in nude mice. DNMT3A induced the methylation of promoter. knockdown reversed the inhibiting effect of silencing on PC cell growth. directly bound to and negatively regulated its expression while up-regulating levels. overexpression reversed the inhibiting effect of overexpression on PC cell growth. In conclusion, the overexpression of could suppress proliferation, invasion, and migration of PC cells, as well as tumor formation in nude mice through inhibiting the methylation of by targeting .

摘要

胰腺癌(PC)是最致命的恶性肿瘤之一,其诊断和预后都很差。已经有报道称在各种癌症中是一种肿瘤抑制因子,而在 PC 的进展过程中 的机制仍知之甚少。在这项研究中,发现 在 PC 中下调,而 上调。下调 或过表达 可抑制 PC 细胞增殖、侵袭和迁移,并在裸鼠中抑制肿瘤形成。DNMT3A 诱导 启动子的甲基化。 下调逆转了 沉默对 PC 细胞生长的抑制作用。 直接与 结合并负调控其表达,同时上调 水平。 过表达逆转了 过表达对 PC 细胞生长的抑制作用。总之,通过靶向 抑制 , 过表达可抑制 PC 细胞的增殖、侵袭和迁移,并在裸鼠中抑制肿瘤形成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b26d/10128082/44b0b64f6f70/LSA-2022-01703_Fig1.jpg

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