دورية أكاديمية

Advances in molecular function of UPF1 in Cancer.

التفاصيل البيبلوغرافية
العنوان: Advances in molecular function of UPF1 in Cancer.
المؤلفون: Temaj G; Faculty of Pharmacy, College UBT, 10000, Prishtina, Republic of Kosovo. Electronic address: gazmend.temaj@ubt-uni.net., Chichiarelli S; Department of Biochemical Sciences 'A. Rossi-Fanelli', Sapienza University of Rome, 00185, Rome, Italy. Electronic address: silvia.chichiarelli@uniroma1.it., Telkoparan-Akillilar P; Department of Medical Biology, Faculty of Medicine, Gazi University, 06500, Ankara, Turkey. Electronic address: pelintelkoparanakillilar@gazi.edu.tr., Saha S; Department of Biotechnology, Institute of Applied Sciences & Humanities, GLA University, Mathura, Uttar Pradesh, India. Electronic address: sarmistha_pharmacol@yahoo.com., Nuhii N; Department of Pharmacy, Faculty of Medical Sciences, State University of Tetovo, 1200, Tetovo, Macedonia. Electronic address: nexhibe.nuhii@unite.edu.mk., Hadziselimovic R; Faculty of Science, University of Sarajevo, 71000, Sarajevo, Bosnia and Herzegovina. Electronic address: rifat.hadziselimovic@gmx.net., Saso L; Department of Physiology and Pharmacology 'Vittorio Erspamer', La Sapienza University, 00185, Rome, Italy. Electronic address: luciano.saso@uniroma1.it.
المصدر: Archives of biochemistry and biophysics [Arch Biochem Biophys] 2024 Jun; Vol. 756, pp. 109989. Date of Electronic Publication: 2024 Apr 14.
نوع المنشور: Journal Article; Review
اللغة: English
بيانات الدورية: Publisher: Elsevier Country of Publication: United States NLM ID: 0372430 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1096-0384 (Electronic) Linking ISSN: 00039861 NLM ISO Abbreviation: Arch Biochem Biophys Subsets: MEDLINE
أسماء مطبوعة: Publication: <2000- > : San Diego, CA : Elsevier
Original Publication: New York, NY : Academic Press
مواضيع طبية MeSH: Neoplasms*/genetics , Neoplasms*/metabolism , Neoplasms*/pathology , RNA Helicases*/metabolism , RNA Helicases*/genetics , Trans-Activators*/metabolism , Trans-Activators*/genetics , Nonsense Mediated mRNA Decay*, Humans ; Gene Expression Regulation, Neoplastic ; Animals ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism
مستخلص: It is known that more than 10 % of genetic diseases are caused by a mutation in protein-coding mRNA (premature termination codon; PTC). mRNAs with an early stop codon are degraded by the cellular surveillance process known as nonsense-mediated mRNA decay (NMD), which prevents the synthesis of C-terminally truncated proteins. Up-frameshift-1 (UPF1) has been reported to be involved in the downregulation of various cancers, and low expression of UPF1 was shown to correlate with poor prognosis. It is known that UPF1 is a master regulator of nonsense-mediated mRNA decay (NMD). UPF1 may also function as an E3 ligase and degrade target proteins without using mRNA decay mechanisms. Increasing evidence indicates that UPF1 could serve as a good biomarker for cancer diagnosis and treatment for future therapeutic applications. Long non-coding RNAs (lncRNAs) have the ability to bind different proteins and regulate gene expression; this role in cancer cells has already been identified by different studies. This article provides an overview of the aberrant expression of UPF1, its functional properties, and molecular processes during cancer for clinical applications in cancer. We also discussed the interactions of lncRNA with UPF1 for cell growth during tumorigenesis.
(Copyright © 2024 Elsevier Inc. All rights reserved.)
فهرسة مساهمة: Keywords: Cancer; Long non-coding RNAs (lncRNAs); Up-frameshift-1 (UPF1)
المشرفين على المادة: EC 3.6.4.13 (RNA Helicases)
EC 3.6.4.13 (UPF1 protein, human)
0 (Trans-Activators)
0 (RNA, Long Noncoding)
تواريخ الأحداث: Date Created: 20240415 Date Completed: 20240513 Latest Revision: 20240710
رمز التحديث: 20240711
DOI: 10.1016/j.abb.2024.109989
PMID: 38621446
قاعدة البيانات: MEDLINE