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真核生物翻译起始因子3亚基B是胰腺癌发生发展的一个促进因子。

Eukaryotic Translation Initiation Factor 3 Subunit B Is a Promoter in the Development and Progression of Pancreatic Cancer.

作者信息

Ren Haoyuan, Mai Gang, Liu Yong, Xiang Rongchao, Yang Chong, Su Wenjie

机构信息

Department of Gastrointestinal Surgery, People's Hospital of Deyang City, Deyang, China.

Organ Transplantation Center, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.

出版信息

Front Oncol. 2021 Apr 29;11:644156. doi: 10.3389/fonc.2021.644156. eCollection 2021.

Abstract

Pancreatic cancer (PC) is a malignant tumor with hidden incidence, high degree of malignancy, rapid disease progression, and poor prognosis. Eukaryotic translation initiation factor 3 subunit B (EIF3B) is necessary for tumor growth, which is an alternative therapeutic target for many cancers. However, little is known about the relationship between EIF3B and PC. The expression of EIF3B in PC was detected by immunohistochemistry. EIF3B knockdown cell models were constructed by lentivirus infection. The MTT assay, the wound-healing assay, the transwell assay, the flow cytometry, and the Human Apoptosis Antibody Array was used to detect the effects of EIF3B knockdown on cell proliferation, cell migration, cell apoptosis, and cell cycle . Also, the effects of EIF3B knockdown on the tumor growth of PC were determined . This study showed that the expression level of EIF3B was significantly up-regulated in PC tumor tissues and associated with pathological grade. , EIF3B knockdown inhibited the PC cell proliferation and migration, and the apoptosis levels were obviously promoted by regulating apoptosis-related proteins including Bcl-2, HSP27, HSP60, Survivin, sTNF-R2, TNF-α, TNF-β, TRAILR-3, TRAILR-4, and XIAP. Furthermore, the tumor growth of PC was inhibited after the knockdown of EIF3B . EIF3B was up-regulated in PC and was a promoter in the development and progression of PC, which could be considered as a therapeutic target for the treatment of PC.

摘要

胰腺癌(PC)是一种发病率隐匿、恶性程度高、疾病进展迅速且预后较差的恶性肿瘤。真核生物翻译起始因子3亚基B(EIF3B)是肿瘤生长所必需的,它是许多癌症的一个潜在治疗靶点。然而,关于EIF3B与PC之间的关系知之甚少。通过免疫组织化学检测PC中EIF3B的表达。通过慢病毒感染构建EIF3B敲低细胞模型。采用MTT法、伤口愈合试验、Transwell试验、流式细胞术和人凋亡抗体阵列检测EIF3B敲低对细胞增殖、细胞迁移、细胞凋亡和细胞周期的影响。此外,还确定了EIF3B敲低对PC肿瘤生长的影响。本研究表明,EIF3B在PC肿瘤组织中的表达水平显著上调,并与病理分级相关。EIF3B敲低抑制了PC细胞的增殖和迁移,通过调节包括Bcl-2、HSP27、HSP60、Survivin、sTNF-R2、TNF-α、TNF-β、TRAILR-3、TRAILR-4和XIAP在内的凋亡相关蛋白,明显促进了细胞凋亡水平。此外,EIF3B敲低后PC的肿瘤生长受到抑制。EIF3B在PC中上调,是PC发生发展的促进因子,可被视为PC治疗的一个靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0c1b/8116711/142f8a7bedb4/fonc-11-644156-g0001.jpg

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