LINC01605
LINC01605, long intergenic non-protein coding RNA 1605, serves a key role in the regulation of important pathways in colon cancer.
Contents
Annotated Information
Name
LINC01605: long intergenic non-protein coding RNA 1605 (HGNC:51654)
Alias
TCONS_00014973; LincDUSP (HGNC:51654)
Characteristics
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. [1]
Function
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.[1] 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. [2]
Regulation
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.[1]
Expression
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. [1]
Diseases
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
References
- ↑ 1.0 1.1 1.2 1.3 1.4 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.
- ↑ 2.0 2.1 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.
Sequence
>gi|100507420|ref|NR_121620.1| Homo sapiens long intergenic non-protein coding RNA 1605 (LINC01605), transcript variant 1, long non-coding RNA
000081 GATGAAGAGC TCGGGTATCT GAGGGCTGGT GTGTCTGCAT GCGTGTGTGT TTTGGGGGCC GACTGAAGGA AGAGAAGGCT 000160
000161 GGAGAGAGGG AACATGGGTC TGAGGGCACA TCGCTAAGGG GTCAAGAGGC CTAAAGGAGG AGTCTAAGGC TCTCCATCGA 000240
000241 ACTTGGACTT GGTCTACATT AGACTTTAAC CTCCATGAGG CTTGGACTTT CAGGCTTCCT CCCTCACACC GCGGGCAGGT 000320
000321 GAGGCGTCTG CTACAGGCCT GGTCTCGCAG AGGGGGCCCA GCGCCCCCCG CCGCCGCCTT CTCCTGGAGT CTGTGTGACA 000400
000401 GAATGGGACC TGTGGGAAAG CAGCACGTCA GCACCCAGCC CCGCTTGCGC GCCAGCAGCT AATTAAAGCC AGGAAGGTGA 000480
000481 TGGCGATTTT CAACTCATTC CCGTTACAAA CAGCCGACCT TCCTACCGAG TTCAAGTACC TTCTGCCTGG CCTGGAAGAA 000560
000561 CAATATCTCT CTGTCTCCCT CTTCCACTGG CCCTCACCTG CCTTCCCCTG AACATGCATT TTGCCTGACA GGAGACAGAG 000640
000641 GCAGTTGAGA TGGAGTCTTG CTATATGGCC CAGCTGGTAA TGCCTAGATT CTTGAGTCCC TCCCTGGCTC ATCCCTGGGA 000720
000721 GCAGCACTGA ACCCCTTGTC TGACACCTGT CTGGAAATGG AGCCTGCACA TTGACCCTAG CCATGTGTGG TCTTGTTACT 000800
000801 AAGTGTTAGC CAGTGAGAGA ACATACAAGA GGAGGCCCAT GTTGATTCAG AGGATGAATG AGAGATGCTT GCAGCTTGGT 000880
000881 CCAGGAGGCC AGCAGGACCA GAGAGAAGAC CACAGCGACA CATGGGGATG GCTGTCCCAC AGGCAGAAAT GAGCAGCCGG 000960
000961 GAGGAAGCCC AGGCAGCCAG CCACCCAGCT CCCTCCACAT CGTGGCCCTA GAACGGAGTC TTGAAGAATA AGAAGCCACA 001040
001041 GCTTGTCAGG GAATCAGGCT GGAAAAATGT TATGAGACTG AGTAAGACCA GAGATTCCTC AGCAGTGCCT GGAGAAGACC 001120
001121 AGGAGAGGAA GCAGAAGACC CTCCTCAAAG AAGCAGCCTT CACCTCCAGA CCTCCCAGCG GGACTTAGAC AATGGGGTTA 001200
001201 GGCAGTCACA TGTCTGCACG TGGAAACTTT CTGGGACTGT GCTTGGATCC TGGCTCTGCC TTTTACTAGC CATGTGACCT 001280
001281 TGGGAAAATC ACTTGACTTC TCCGTGCAGG ATTCCTCATC TGTAAAAATG GTCTAAGATT AGGAGCCACC TCAAGGTTGT 001360
001361 TGTAGGAATT AAATTAATTC ATGTTTATAA AGTGCTTTGA ACAGCGTTTG GCACATGGTA AGTGCTATGT GGTAAGTGCT 001440
001441 GTCTATTGAT TACATAAATA AAAGTGATCA CCATTAGACT TTCCATGCAG ATGATATTAT GCATATACAT ATCTCCCGCA 001520
001521 TATGACGTCA TTGGATCGTT TTGCAATGGT GGGGGGTTTA TTCTTTTCCT TTTTGTTTTC TTCTTTTTTT TGTCAGATGA 001600
001601 AGAAACTGAT GGGAAGTGAA TTGGTTTGTA TTAAACATTA GGTTTGCTAA AAAAAAAAAA AAA
