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Cancer Lett. 2019 Jun 7;459:112-121. doi: 10.1016/j.canlet.2019.114430. [Epub ahead of print]

CFIm25 and alternative polyadenylation: Conflicting roles in cancer.

Author information

1
Department of Medical Biotechnology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. Electronic address: mohammadhassanj@gmail.com.
2
Research Center for Biochemistry and Nutrition in Metabolic Diseases, Kashan University of Medical Sciences, Kashan, Iran. Electronic address: r.shafabakhsh@gmail.com.
3
Research Center for Biochemistry and Nutrition in Metabolic Diseases, Kashan University of Medical Sciences, Kashan, Iran. Electronic address: Asemi_r@yahoo.com.
4
Department of Medical Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: h-mirzaei@tums.ac.ir.
5
Department of Molecular Medicine, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran. Electronic address: rsahebnasagh@razi.tums.ac.ir.
6
Research Center for Biochemistry and Nutrition in Metabolic Diseases, Kashan University of Medical Sciences, Kashan, Iran. Electronic address: h.mirzaei2002@gmail.com.
7
Wellman Center for Photomedicine, Massachusetts General Hospital, Harvard Medical School, 40 Blossom Street, Boston, MA, 02114, USA. Electronic address: hamblin@helix.mgh.harvard.edu.

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.

KEYWORDS:

Alternative polyadenylation; CFIm25; Cancer; Competing endogenous RNAs; MicroRNA

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