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敲低真核生物翻译起始因子3a(eIF3a)可减弱K1人甲状腺癌细胞的生长。

Knockdown of eIF3a attenuated cell growth in K1 human thyroid cancer cells.

作者信息

Zheng Xucai, Wang Shengying, Hong Shikai, Liu Jianjun, Jiang Chenghao

机构信息

Department of Head and Neck, Breast Surgery, the First Affiliated Hospital of University of Science and Technology of China, Anhui Provincial Cancer Hospital, No.107 Huanhu East Road, Hefei, 230001, China.

出版信息

Genes Genomics. 2021 Apr;43(4):379-388. doi: 10.1007/s13258-021-01048-5. Epub 2021 Feb 17.

Abstract

BACKGROUND

In ribosome establishment and the initiation of translation, eukaryotic translation initiation factor (eIF) 3a is a pivotal functional subunit of the eIF3 complex. In various cancer types, abnormal eIF3a expression plays an important role in tumorigenesis.

OBJECTIVE

We aimed to explore the role of eIF3a in human thyroid cancer (TC).

MATERIAL AND METHODS

The expression of eIF3a was determined in TC tissues by qRT-PCR and immunohistochemistry (IHC) assay, respectively. In addition, the expression of eIF3a in K1 and BCPAP cells were detected by qRT-PCR. Cell proliferation, cell cycle, and cell apoptosis were assessed after eIF3a knockdown in K1 in cell line.

RESULTS

The expression of eIF3a mRNA was high in TC tissues and cancer cell lines. Moreover, eIF3a expression in TC tissues indicated that high eIF3a level was associated with tumor grade. In addition, eIF3a knockdown resulted in a significantly decrease in cell proliferation and increased the apoptosis of K1 cells. Cell cycle was arrested in both the S and G2/M phase. The levels of phosphorylated ERK1/2 and surviving were decreased after eIF3a knockdown.

CONCLUSION

Our study suggested that eIF3a contributed to TC cell proliferation. It may be a promising target for gene therapy in human thyroid cancer.

摘要

背景

在核糖体的形成及翻译起始过程中,真核生物翻译起始因子(eIF)3a是eIF3复合体的关键功能亚基。在多种癌症类型中,eIF3a表达异常在肿瘤发生过程中发挥重要作用。

目的

我们旨在探究eIF3a在人甲状腺癌(TC)中的作用。

材料与方法

分别通过qRT-PCR和免疫组织化学(IHC)检测法测定TC组织中eIF3a的表达。此外,通过qRT-PCR检测K1和BCPAP细胞中eIF3a的表达。在细胞系K1中敲低eIF3a后,评估细胞增殖、细胞周期和细胞凋亡情况。

结果

eIF3a mRNA在TC组织和癌细胞系中高表达。此外,TC组织中的eIF3a表达表明,eIF3a高表达水平与肿瘤分级相关。此外,敲低eIF3a导致细胞增殖显著降低,并增加了K1细胞的凋亡。细胞周期阻滞在S期和G2/M期。敲低eIF3a后,磷酸化ERK1/2和存活蛋白的水平降低。

结论

我们的研究表明,eIF3a促进TC细胞增殖。它可能是人类甲状腺癌基因治疗的一个有前景的靶点。

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