BCYRN1: An oncogenic lncRNA in diverse cancers

Ghafouri‐Fard, Soudeh; Dashti, Sepideh; Hussen, Bashdar Mahmud; Farsi, Molood; Taheri, Mohammad

doi:10.1016/j.prp.2021.153385

Cited by 13 publications

(10 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…6h ). BC200 ncRNA, which also presents evidence of gene-level correlation with POLR3G availability, has been similarly reported to be enhanced by MYC and essential for viability and proliferation in cancer contexts 23 , 24 , 87 – 90 . In addition to snaR-A and BC200, we find that specific tRNA genes are sensitive to POLR3G disruption, including tRNA-Ala genes recently shown to be sensitive to MYC depletion in human HEK293 cells 91 .…”

Section: Discussionmentioning

confidence: 95%

A cancer-associated RNA polymerase III identity drives robust transcription and expression of snaR-A noncoding RNA

et al. 2022

View full text Add to dashboard Cite

RNA polymerase III (Pol III) includes two alternate isoforms, defined by mutually exclusive incorporation of subunit POLR3G (RPC7α) or POLR3GL (RPC7β), in mammals. The contributions of POLR3G and POLR3GL to transcription potential has remained poorly defined. Here, we discover that loss of subunit POLR3G is accompanied by a restricted repertoire of genes transcribed by Pol III. Particularly sensitive is snaR-A, a small noncoding RNA implicated in cancer proliferation and metastasis. Analysis of Pol III isoform biases and downstream chromatin features identifies loss of POLR3G and snaR-A during differentiation, and conversely, re-establishment of POLR3G gene expression and SNAR-A gene features in cancer contexts. Our results support a model in which Pol III identity functions as an important transcriptional regulatory mechanism. Upregulation of POLR3G, which is driven by MYC, identifies a subgroup of patients with unfavorable survival outcomes in specific cancers, further implicating the POLR3G-enhanced transcription repertoire as a potential disease factor.

show abstract

Section: Discussionmentioning

confidence: 95%

A cancer-associated RNA polymerase III identity drives robust transcription and expression of snaR-A noncoding RNA

et al. 2022

View full text Add to dashboard Cite

show abstract

“…Previous study reported that BCYRN1 was an oncogenic lncRNA contributing to the progression of various cancers by serving as a crucial microRNA sponge. 42 Overexpression of BCYRN1 competitively bound with miR-204-3p to regulate the tumorigenesis of colorectal cancer. 43 However, the biological role of BCYRN1 in exosome-induced LN Feedforward loop is a critical manner for the regulation of transcription networks during tumor progression.…”

Section: Discussionmentioning

confidence: 99%

Tumor‐derived exosomal BCYRN1 activates WNT5A/VEGF‐C/VEGFR3 feedforward loop to drive lymphatic metastasis of bladder cancer

Zheng

Chen

Luo

et al. 2021

Clinical & Translational Med

View full text Add to dashboard Cite

lncRNA BCYRN1 is upregulated in urinary exosomes from bladder cancer (BCa) patients and associated with LN metastasis and poor prognosis of patients. BCYRN1 upregulates WNT5A expression to activate WNT/β-catenin pathway and promotes the secretion of VEGF-C in BCa. Exosomal BCYRN1 stabilizes VEGFR3 mRNA in HLECs, constituting a feedforward loop to promote lymphangiogenesis and LN metastasis of BCa.

show abstract

“…LncRNAs are defined as transcripts of more of 200 nucleotides and containing little or no protein-coding potential. They are involved in the transcriptional and post-transcriptional regulation of various biological processes involved in tumor development [reviewed in [ 47 ]]. It has been shown that BC200 promotes the expression of matrix metalloproteinases 9 and 13 (MMP9 and MMP13) [ 48 ], two matrix metalloproteinases that catalyze the degradation of extracellular matrix (ECM) components responsible of the cleavage and release of biologically active molecules stored in the ECM, such as vascular endothelial growth factor A (VEGFA).…”

Section: Signal Transductionmentioning

confidence: 99%

Complex and pleiotropic signaling pathways regulated by the secreted protein augurin

2023

View full text Add to dashboard Cite

The secreted protein augurin, the product of the tumor suppressor gene Ecrg4, has been identified as a peptide hormone in the human proteome in 2007. Since then, a number of studies have been carried out to highlight its structure and processing and its potential roles in physiopathology. Although augurin has been shown to be implicated in a variety of processes, ranging from tumorigenesis, inflammation and infection to neural stem cell proliferation, hypothalamo-pituitary adrenal axis regulation and osteoblast differentiation, the molecular mechanisms of its biological effects and the signaling pathways it regulates are still poorly characterized. Here we provide a comprehensive overview of augurin-dependent signal transduction pathways. Because of their secreted nature and the potential to be manipulated pharmacologically, augurin and its derived peptides represent attractive targets for diagnostic development and discovery of new therapeutic agents for the human diseases resulting from the deregulation of the signaling cascades they modulate. From this perspective, the characterization of the precise nature of augurin derived peptides and the identification of the receptor(s) on the cell surface conveying augurin signaling to downstream effectors are crucial to develop agonists and antagonists for this protein.

show abstract

BCYRN1: An oncogenic lncRNA in diverse cancers

Cited by 13 publications

References 28 publications

A cancer-associated RNA polymerase III identity drives robust transcription and expression of snaR-A noncoding RNA

A cancer-associated RNA polymerase III identity drives robust transcription and expression of snaR-A noncoding RNA

Tumor‐derived exosomal BCYRN1 activates WNT5A/VEGF‐C/VEGFR3 feedforward loop to drive lymphatic metastasis of bladder cancer

Complex and pleiotropic signaling pathways regulated by the secreted protein augurin

Contact Info

Product

Resources

About