Abstract
Long non-coding RNAs (LncRNAs) can bind to other proteins or RNAs to regulate gene expression, and its role in tumors has been extensively studied. A common RNA binding protein, UPF1, is also a key factor in a variety of RNA decay pathways. RNA decay pathways serve to control levels of particular RNA molecules. The expression of UPF1 is often dysregulated in tumors, an observation which suggests that UPF1 contributes to development of a variety of tumors. Herein, we review evidence from studies of fourteen lncRNAs interact with UPF1. The interaction between lncRNA and UPFI provide fundamental basis for cell transformation and tumorigenic growth.
Highlights
About 93% of the human genome is transcribed into RNA
There are three possible mechanisms for cis action: (1) lncRNA recruits transcription factors to a locus to regulate the expression of a nearby gene (Figure 1A); (2) regulation of nearby genes during lncRNA transcription and shearing (Figure 1B); and (3) regulation of nearby genes by the lncRNA promoter or original DNA of the locus (Figure 1C; Ma et al, 2013; Kopp and Mendell, 2018; Yao et al, 2019)
The lncRNA GAS5 interacts with the WW domain of the YAP protein in colorectal cancer, and promotes the degradation of Yes1-related transcriptional regulators (YAP) through the ubiquitin-proteasome pathway (Ni et al, 2019)
Summary
About 93% of the human genome is transcribed into RNA. Protein-coding genes account for only about 2% of RNAs, with the vast majority of transcripts being non-coding RNAs (ncRNAs) (Qian et al, 2019). The lncRNA GAS5 interacts with the WW domain of the YAP protein in colorectal cancer, and promotes the degradation of Yes1-related transcriptional regulators (YAP) through the ubiquitin-proteasome pathway (Ni et al, 2019). LncRNAs Bind UPF1 and Affect the Stability of mRNA
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
