Difference between revisions of "LINC01605"
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LINC01605, long intergenic non-protein coding RNA 1605, serves a key role in the regulation of important pathways in colon cancer.
LINC01605: long intergenic non-protein coding RNA 1605 (HGNC:51654)
TCONS_00014973; LincDUSP (HGNC:51654)
LincDUSP (Gene Symbol: LINC01605, RefSeq: NR_121621.1) is located at 8p11.23 and spans 4981 bp in the genome. The mature RNA consists of 3 exons totaling 528 bp. Importantly, lincDUSP was not shown to contain small ORFs based on a large-scale study of human lincRNAs, providing supportive evidence that this RNA does not encode small peptides. 
LINC01605 or lincDUSP, is a potential candidate oncogene. Subcellular RNA isolation demonstrated that lincDUSP is enriched in the nucleus, suggesting that lincDUSP may play a role in gene regulation via interaction with chromatin. lincDUSP mediate long-range chromatin looping. Notably, lincDUSP ChIRP-seq showed chromatin occupancy near EXO1, PCNA, and RFC3, which are known to be involved in replication-associated DNA repair. lincDUSP regulates gene expression by enabling interaction between cis-regulatory elements and gene promoters. LINC01605 has been found to be up-regulated in bladder cancer (BC) tissues compared with normal tissues and as a new prognostic biomarker, could promote the proliferation, migration, and invasion of BC cells via activating EMT signaling pathway and up-regulating MMP9 expression. 
Currently, the clinical and genetic factors that distinguish colon tumors with lincDUSP overexpression from other colon tumors with more modest expression are unclear; indeed, it is also unknown how lincDUSP becomes overexpressed in this context. Proposed mechanisms of lncRNA dysregulation include locus amplification (similar to HER2 amplification in breast cancer); large-scale DNA mutations such as deletions, insertions, and translocations; or smaller-scale deletions at critical functional regions within the lncRNA sequence. Further exploration of these mechanisms will aid in understanding the role of lncRNA dysregulation in disease pathogenesis.
lincDUSP is expressed in several normal tissues in humans including colon, breast, and lung. lincDUSP expression is associated with increased proliferation and enhanced clonogenic potential. Knockdown of lincDUSP increases the susceptibility of colon cancer cells to apoptosis. Specifically, lincDUSP expression is consistently modest in normal colon but is significantly upregulated in colon tumors. 
Labs working on this lncRNA
- Department of Genetics and Genome Sciences, Cleveland, OH 44106 USA
- Case Comprehensive Cancer Center, Cleveland, OH 44106 USA
- Department of Biochemistry, Case Western Reserve University, Cleveland, OH 44106 USA
- Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210009, China
- Department of Urology, Jiangsu Province Hospital of TCM, Affiliated Hospital of Nanjing University of TCM, Nanjing 210029, China
- Department of Urology, Affiliated Hospital of Nantong University, Nantong 226001, China
- Forrest ME, Saiakhova A, Beard L, Buchner DA, Scacheri PC, LaFramboise T et al. Colon Cancer-Upregulated Long Non-Coding RNA lincDUSP Regulates Cell Cycle Genes and Potentiates Resistance to Apoptosis[J]. Scientific Reports. 2018, 8(1):7324-7324.
- Qin Z, Wang Y, Tang J, Zhang L, Li R, Xue J et al. High LINC01605 expression predicts poor prognosis and promotes tumor progression via up-regulation of MMP9 in bladder cancer[J]. Bioscience reports. 2018, 38(5):BSR20180562.
>gi|100507420|ref|NR_121620.1| Homo sapiens long intergenic non-protein coding RNA 1605 (LINC01605), transcript variant 1, long non-coding RNA