Interaction Between LncRNA and UPF1 in Tumors

He, Jiaxi; Ma, Xiaoxin

doi:10.3389/fgene.2021.624905

Cited by 13 publications

(7 citation statements)

References 64 publications

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“…Among them, UPF1 regulates other pathways including replication-dependent histone mRNA decay (HMD). In the NMD, UPF1 binds to the premature stop codon (PTC) via a translation termination complex bound [ 26 , 27 ]. The NMD can recognize post-transcriptionally aberrant transcripts and mediate their degradation.…”

Section: Discussionmentioning

confidence: 99%

The biological behavior of tRNA-derived fragment tRF-Leu-AAG in pancreatic cancer cells

et al. 2022

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Pancreatic cancer (PC) is a life-threatening cancer with increasing incidence in developed countries. Reports indicate that tRNA-derived fragments (tRFs) are possible therapeutic targets and biomarkers for cancer treatment. Nonetheless, the effect of tRF-Leu-AAG on PC is unclear. This study aims to explore the role of tRF-Leu-AAG and upstream frameshift mutant 1 (UPF1) in the development of PC and its potential underlying mechanisms. High-throughput second-generation sequencing techniques were used to detect the expression of tRFs in cancerous and adjacent normal tissues from PC patients. The role of tRF-Leu-AAG proliferation in PC cells was investigated via the Cell Counting Kit-8 (CCK8) assay. The effect of tRF-Leu-AAG on the invasion and migration ability of PC cells was also determined by the transwell assay. Thereafter, the downstream target genes of tRF-Leu-AAG were comprehensively predicted using bioinformatics analysis databases. We also used the Dual-Luciferase Reporter assay to assess the nexus between tRF-Leu-AAG and UPF1. Eventually, Western Blot was used to validate the expression of UPF1 in PC cells. A total of 33 tRF expressions significantly varied from PC patients. RT-qPCR confirmed that the expression of tRF-Leu-AAG was observably up-regulated in PC cells as compared to the control cells. Importantly, knockdown of tRF-Leu-AAG observably inhibited cell proliferation, migration, and invasion. Furthermore, according to the predicted frameshift database results, the UPF1 acted as downstream target genes for tRF-Leu-AAG and significantly down-regulated UPF1 expression.

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Section: Discussionmentioning

confidence: 99%

The biological behavior of tRNA-derived fragment tRF-Leu-AAG in pancreatic cancer cells

et al. 2022

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“…Different lncRNAs have been shown to interact with G3BP1 [ 55 , 56 ], UPF1 [ 37 , 57 , 58 , 59 ] and MOV10 [ 37 ]. In contrast to these studies, which focus on, and elucidate, the individual interaction case-specifically, we, for the first time, have reported on a lncRNA to control mRNA turnover by being a crucial structural component of cytoplasmic G3BP1-positive RNPs ( Figure 4 ).…”

Section: Discussionmentioning

confidence: 99%

The G3BP1-UPF1-Associated Long Non-Coding RNA CALA Regulates RNA Turnover in the Cytoplasm

Kirchhof

Fouani

Knau

et al. 2022

ncRNA

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Besides transcription, RNA decay accounts for a large proportion of regulated gene expression and is paramount for cellular functions. Classical RNA surveillance pathways, like nonsense-mediated decay (NMD), are also implicated in the turnover of non-mutant transcripts. Whereas numerous protein factors have been assigned to distinct RNA decay pathways, the contribution of long non-coding RNAs (lncRNAs) to RNA turnover remains unknown. Here we identify the lncRNA CALA as a potent regulator of RNA turnover in endothelial cells. We demonstrate that CALA forms cytoplasmic ribonucleoprotein complexes with G3BP1 and regulates endothelial cell functions. A detailed characterization of these G3BP1-positive complexes by mass spectrometry identifies UPF1 and numerous other NMD factors having cytoplasmic G3BP1-association that is CALA-dependent. Importantly, CALA silencing impairs degradation of NMD target transcripts, establishing CALA as a non-coding regulator of RNA steady-state levels in the endothelium.

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“…25 Furthermore, Xrn1 in the cytoplasm or exosomes containing Nrd1-Nab3-Sen1 and TRAMP assemblies in the nucleus facilitate the breakdown of lncRNA, while nonsense-mediated decay protein UPF1 inhibits this process. 26 These results imply that the adjustment of lncRNA synthesis is significantly influenced by epigenetic changes. The specific mechanisms remain not fully understood, though.…”

Section: Overview Of Lncrnasmentioning

confidence: 92%

“…The imprinted gene cluster's lncRNA Air transcription is strongly inhibited through the methylation of the paternal allele, which in turn activates the expression of neighboring protein‐coding genes such as Igf2r, Slc22a2, and Slc22a3 25 . Furthermore, Xrn1 in the cytoplasm or exosomes containing Nrd1‐Nab3‐Sen1 and TRAMP assemblies in the nucleus facilitate the breakdown of lncRNA, while nonsense‐mediated decay protein UPF1 inhibits this process 26 . These results imply that the adjustment of lncRNA synthesis is significantly influenced by epigenetic changes.…”

Section: Overview Of Lncrnasmentioning

confidence: 99%

The role of long noncoding RNA DGCR5 in cancers: Focus on molecular targets

Al‐Hawary,

Rodrigues,

Bangali

et al. 2024

Cell Biochemistry & Function

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Long noncoding RNAs (lncRNAs) are major components of cellular transcripts that are emerging as important players in various biological pathways. Due to their specific expression and functional diversity in a variety of cancers, lncRNAs have promising applications in cancer diagnosis, prognosis, and therapy. Studies have shown that lncRNA DiGeorge syndrome critical region gene 5 (DGCR5) with high specificity and accuracy has the potential to become biomarkers in cancers. LncRNA DGCR5 can be noninvasively extracted from body fluids, tissues, and cells, and can be used as independent or auxiliary biomarkers to improve the accuracy of diagnosis or prognosis. Now, the underlying mechanisms of lncRNAs such as DGCR5 were explored as therapeutic targets, which have been investigated in clinical trials of several cancers. The DGCR5 lacks an appropriate animal model, which is necessary to gain greater knowledge of their functions. While some studies on the uses of DGCR5 have been carried out, the small sample size makes them unreliable. In this review, we presented a compilation of recent publications addressing the potential of lncRNA DGCR5 that could be considered as biomarkers or therapeutic targets, with the hopes of providing promised implications for future cancer therapy.

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Interaction Between LncRNA and UPF1 in Tumors

Cited by 13 publications

References 64 publications

The biological behavior of tRNA-derived fragment tRF-Leu-AAG in pancreatic cancer cells

The biological behavior of tRNA-derived fragment tRF-Leu-AAG in pancreatic cancer cells

The G3BP1-UPF1-Associated Long Non-Coding RNA CALA Regulates RNA Turnover in the Cytoplasm

The role of long noncoding RNA DGCR5 in cancers: Focus on molecular targets

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