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CFIm25 和可变多聚腺苷酸化:在癌症中的矛盾作用。

CFIm25 and alternative polyadenylation: Conflicting roles in cancer.

机构信息

Department of Medical Biotechnology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.

Research Center for Biochemistry and Nutrition in Metabolic Diseases, Kashan University of Medical Sciences, Kashan, Iran.

出版信息

Cancer Lett. 2019 Sep 10;459:112-121. doi: 10.1016/j.canlet.2019.114430. Epub 2019 Jun 7.

Abstract

Alternative polyadenylation (APA) is now widely recognized to regulate gene expression. APA is an RNA-processing mechanism that generates distinct 3' termini on mRNAs, producing mRNA isoforms. Different factors influence the initiation and development of this process. CFIm25 (among others) is a cleavage and polyadenylation factor that plays a key role in the regulation of APA. Shortening of the 3'UTRs on mRNAs leads to enhanced cellular proliferation and tumorigenicity. One reason may be the up-regulation of growth promoting factors, such as Cyclin D1. Different studies have reported a dual role of CFIm25 in cancer (both oncogenic and tumor suppressor). microRNAs (miRNAs) may be involved in CFIm25 function as well as competing endogenous RNAs (ceRNAs). The present review focuses on the role of CFIm25 in cancer, cancer treatment, and possible involvement in other human diseases. We highlight the involvement of miRNAs and ceRNAs in the function of CFIm25 to affect gene expression. The lack of understanding of the mechanisms and regulation of CFIm25 and APA has underscored the need for further research regarding their role in cancer and other diseases.

摘要

可变多聚腺苷酸化(APA)现在被广泛认为是调节基因表达的一种机制。APA 是一种 RNA 加工机制,它在 mRNA 上产生不同的 3'末端,产生 mRNA 异构体。不同的因素影响这个过程的起始和发展。CFIm25(以及其他)是一种切割和多聚腺苷酸化因子,在 APA 的调节中起着关键作用。mRNA 3'UTR 的缩短导致细胞增殖和致瘤性增强。一个原因可能是生长促进因子(如 Cyclin D1)的上调。不同的研究报告表明 CFIm25 在癌症中具有双重作用(致癌和肿瘤抑制)。microRNAs(miRNAs)可能参与 CFIm25 的功能以及竞争性内源 RNA(ceRNA)。本文综述了 CFIm25 在癌症、癌症治疗以及可能涉及其他人类疾病中的作用。我们强调了 miRNAs 和 ceRNAs 参与 CFIm25 功能以影响基因表达。对 CFIm25 和 APA 的机制和调节的理解不足,强调了需要进一步研究它们在癌症和其他疾病中的作用。

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本文引用的文献

1
Cleavage factor 25 deregulation contributes to pulmonary fibrosis through alternative polyadenylation.
J Clin Invest. 2019 Feb 28;129(5):1984-1999. doi: 10.1172/JCI122106. Print 2019 May 1.
2
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Oncogene. 2019 May;38(21):4154-4168. doi: 10.1038/s41388-019-0714-9. Epub 2019 Jan 31.
3
Knockdown of NUDT21 inhibits proliferation and promotes apoptosis of human K562 leukemia cells through ERK pathway.
Cancer Manag Res. 2018 Oct 8;10:4311-4323. doi: 10.2147/CMAR.S173496. eCollection 2018.
4
Alternative polyadenylation confers Pten mRNAs stability and resistance to microRNAs.
Nucleic Acids Res. 2018 Nov 2;46(19):10340-10352. doi: 10.1093/nar/gky666.
5
Suppression of cleavage factor Im 25 promotes the proliferation of lung cancer cells through alternative polyadenylation.
Biochem Biophys Res Commun. 2018 Sep 5;503(2):856-862. doi: 10.1016/j.bbrc.2018.06.087. Epub 2018 Jun 23.
6
3' UTR shortening represses tumor-suppressor genes in trans by disrupting ceRNA crosstalk.
Nat Genet. 2018 Jun;50(6):783-789. doi: 10.1038/s41588-018-0118-8. Epub 2018 May 21.
8
CFIm25 inhibits hepatocellular carcinoma metastasis by suppressing the p38 and JNK/c-Jun signaling pathways.
Oncotarget. 2018 Jan 31;9(14):11783-11793. doi: 10.18632/oncotarget.24364. eCollection 2018 Feb 20.
9
Silencing NUDT21 Attenuates the Mesenchymal Identity of Glioblastoma Cells via the NF-κB Pathway.
Front Mol Neurosci. 2017 Dec 19;10:420. doi: 10.3389/fnmol.2017.00420. eCollection 2017.
10
RNA Binding Protein as an Emerging Therapeutic Target for Cancer Prevention and Treatment.
J Cancer Prev. 2017 Dec;22(4):203-210. doi: 10.15430/JCP.2017.22.4.203. Epub 2017 Dec 30.

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