Entry Detail



General Information

Database ID:LDA0007471
Species:Homo sapiens
Confidence Score:0.9952
Contents:>> ncRNA Information
>> Regulatory Relationship
>> Disease Information
>> Evidence Support
>> Reference

 

ncRNA Information

ncRNA Symbol:XIST
Full Name:X inactive specific transcript (non-protein coding)
Category:lncRNA
Species:Homo sapiens
Synonyms:NCRNA00001//DXS1089//swd66//LINC00001
Chromosome:X
Strand:-
Coordinate:
Start Site(bp):73820651End Site(bp):73852753
Gene Summary:X inactivation is an early developmental process in mammalian females that transcriptionally silences one of the pair of X chromosomes, thus providing dosage equivalence between males and females. The process is regulated by several factors, including a region of chromosome X called the X inactivation center (XIC). The XIC comprises several non-coding and protein-coding genes, and this gene was the first non-coding gene identified within the XIC. This gene is expressed exclusively from the XIC of the inactive X chromosome, and is essential for the initiation and spread of X-inactivation. The transcript is a spliced RNA. Alternatively spliced transcript variants have been identified, but their full length sequences have not been determined. Mutations in the XIST promoter cause familial skewed X inactivation. [provided by RefSeq, Apr 2012]
External Links:
Ensembl ID:ENSG00000229807
HGNC ID:HGNC:12810
Entrez Gene:7503
VEGA ID:OTTHUMG00000021839
UCSC ID:uc004ebm.3
ENA:M97168
RefSeq Accession:NR_001564
UniProtKB:N/A

 

Regulatory Relationship

mRNA targets:N/A
miRNA targets:N/A
Display:N/A

 

Disease Information

 Disease OntologyMeSH
Disease ID:DOID:9256D015179
Disease Name:colorectal cancerColorectal Neoplasms
Category:Disease OntologyMeSH
Type:disease of cellular proliferationNeoplasms//Digestive System Diseases
Define:A large intestine cancer that is located_in the colon and/or located_in the rectum.Tumors or cancer of the COLON or the RECTUM or both. Risk factors for colorectal cancer include chronic ULCERATIVE COLITIS; FAMILIAL POLYPOSIS COLI; exposure to ASBESTOS; and irradiation of the CERVIX UTERI.
Alias:N/ANeoplasms, Colorectal//Colorectal Neoplasm//Neoplasm, Colorectal//Colorectal Tumors//Colorectal Tumor//Tumor, Colorectal//Tumors, Colorectal//Colorectal Carcinoma//Carcinoma, Colorectal//Carcinomas, Colorectal//Colorectal Carcinomas//Colorectal Cancer//Cancer, Colorectal//Cancers, Colorectal//Colorectal Cancers

 

Evidence Support

Strong Evidence:FISH//IF//RT-qPCR//Western blot
Weak Evidence:HiSeq sequencing assay//Microarray
Prediction Method:LRLSLDA-LNCSIM1//LRLSLDA-LNCSIM2

 

Reference

[1] PubMed ID:17143621
Disease Name:colorectal cancer
Sample:CRC tissue
Dysfunction Pattern:Expression [differentially expressed]
Validated Method:FISH//Microarray
Description:X inactive-specific transcript gene amplification has also been detected in microsatellite-unstable sporadic human CRC tissue when compared to matched normal colorectal epithelium. aCGH revealed distinct DNA copy number changes between sporadic CIN- and MIN-associated colorectal carcinomas. A differential role of these candidate oncogenes and tumor suppressor genes in tumor development and progression of sporadic CIN and MIN CRC is likely and may also be involved in the response or resistance to therapeutic interventions,such as shown for microsatellite instability and 5-FU.
Author:Lassmann S,Weis R,Makowiec F,Roth J,Danciu M,Hopt U,Werner M
Year:2007
Title:Array CGH identifies distinct DNA copy number profiles of oncogenes and tumor suppressor genes in chromosomal- and microsatellite-unstable sporadic colorectal carcinomas.
Causality:No

[2] PubMed ID:28730777
Disease Name:colorectal cancer
Sample:CRC cells and 50 pairs of human CRC tissues and adjacent tissues
Dysfunction Pattern:Expression [high expression]
Validated Method:RT-qPCR//Western blot
Description:The expression level of XIST was significantly increased in both CRC tissues sample and CRC cells. XIST promoted CRC cell proliferation by affecting the cell cycle._
Author:Song H,He P,Shao T,Li Y,Li J,Zhang Y
Year:2017
Title:Long non-coding RNA XIST functions as an oncogene in human colorectal cancer by targeting miR-132-3p.
Causality:Yes

[3] PubMed ID:29137332
Disease Name:colorectal cancer
Sample:CRC cell lines
Dysfunction Pattern:Regulation [up-regulated]
Validated Method:RT-qPCR//Western blot//IF//HiSeq sequencing assay
Description:By using the next generation HiSeq sequencing assay, we identified lncRNAs showing differential expression levels in 5FU resistant and non-resistant CRC patients. RT-qPCR was then performed for validation in tissues and serum samples, and lncRNA XIST was verified to be up-regulated in non-responding patients and have considerable diagnostic potential to identify responding patients from non-responding patients. In addition, increased serum XIST level was associated with poor response and lower survival rate in CRC patients receiving 5FU-based treatment. Subsequently, the 5FU resistant (5FU-R) cell lines were established, and lncRNA XIST was significantly up-regulated HT29 5FU-R and HCT116 5FU-R cells. Furthermore, knockdown of XIST reversed 5FU resistance while enhanced XIST could restrained the 5FU-induced cell cytotoxcity in both CRC cell lines. Western blotting and immunofluorescence analysis indicated that XIST promoted the expression of thymidylate synthase, a critical 5FU-targetd enzyme.
Author:Xiao Y,Yurievich UA,Yosypovych SV
Year:2017
Title:Long noncoding RNA XIST is a prognostic factor in colorectal cancer and inhibits 5-fluorouracil-induced cell cytotoxicity through promoting thymidylate synthase expression.
Causality:Yes

[4] PubMed ID:29495975
Disease Name:colorectal cancer
Sample:CRC tissues and CRC cells
Dysfunction Pattern:Regulation [up-regulated]
Validated Method:RT-qPCR
Description:LncRNA XIST was upregulated in CRC tissues. Compared with HT29 cells that had low metastatic potential, XIST was markedly higher expressed in LoVo cells that had higher metastatic potential. Overexpression of XIST promoted the migratory and invasive potential of HT29 cells, while knockdown of XIST inhibited the migratory and invasive potential of LoVo cells. Moreover, epithelial-mesenchymal transition (EMT) markers, including Ecadherin, N-cadherin, and Vimentin, exhibited corresponding expression changes. In addition, miR-137 was inhibited by XIST and inhibition of miR-137 could reverse the effects of knockdown of XIST on the migratory and invasive potential of LoVo cells. Furthermore, enhancer of zeste homolog 2 (EZH2) was confirmed as a target of miR-137.
Author:Liu X,Cui L,Hua D
Year:2018
Title:Long Noncoding RNA XIST Regulates miR-137-EZH2 Axis to Promote Tumor Metastasis in Colorectal Cancer.
Causality:Yes