MALAT 1 (metastasis associated lung adenocarcinoma transcript 1) also known as NEAT2 (noncoding nuclear-enriched abundant transcript 2) is a large, infrequently spliced non-coding RNA, which is highly conserved amongst mammals and highly expressed in the nucleus.[3] It regulates the expression of metastasis-associated genes.[4] It also positively regulates cell motility via the transcriptional and/or post-transcriptional regulation of motility-related genes.[5] MALAT1 may play a role in temperature-dependent sex determination in the Red-eared slider turtle (Trachemys scripta).[6]

MALAT1
Identifiers
AliasesMALAT1, HCN, LINC00047, MALAT-1, NCRNA00047, NEAT2, PRO2853, mascRNA, metastasis associated lung adenocarcinoma transcript 1 (non-protein coding), metastasis associated lung adenocarcinoma transcript 1
External IDsOMIM: 607924; GeneCards: MALAT1; OMA:MALAT1 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

n/a

n/a

RefSeq (protein)

n/a

n/a

Location (UCSC)Chr 11: 65.5 – 65.51 Mbn/a
PubMed search[2]n/a
Wikidata
View/Edit Human
Conserved secondary structure in Metastasis associated lung adenocarcinoma transcript 1
Identifiers
SymbolMALAT1
RfamRF01871
Other data
RNA typeGene;
Domain(s)Eukaryota;
GOGO:2000147
SOSO:0001263
PDB structuresPDBe

Expression in alcoholic brains edit

Transcripts of MALAT1 are significantly increased in the cerebellum of human alcoholics, as well as in similar regions of rat brains after the withdrawal of ethanol vapours. This alcohol-induced upregulation of MALAT1 may be responsible for differential expression of a number of proteins which contribute to ethanol tolerance and dependency in humans.[7]

Prognostic potential in cancer edit

Elevated MALAT1 expression is correlated with poor overall survival in various types of cancer, suggesting that this gene is a prognostic factor for different types of cancer.[8][9]

See also edit

References edit

  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000251562Ensembl, May 2017
  2. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  3. ^ Hutchinson JN, Ensminger AW, Clemson CM, Lynch CR, Lawrence JB, Chess A (2007). "A screen for nuclear transcripts identifies two linked noncoding RNAs associated with SC35 splicing domains". BMC Genomics. 8: 39. doi:10.1186/1471-2164-8-39. PMC 1800850. PMID 17270048.  
  4. ^ Gutschner T, Hämmerle M, Eissmann M, Hsu J, Kim Y, Hung G, Revenko A, Arun G, Stentrup M, Gross M, Zörnig M, MacLeod AR, Spector DL, Diederichs S (February 2013). "The noncoding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells". Cancer Research. 73 (3): 1180–1189. doi:10.1158/0008-5472.CAN-12-2850. PMC 3589741. PMID 23243023.
  5. ^ Tano K, Mizuno R, Okada T, Rakwal R, Shibato J, Masuo Y, Ijiri K, Akimitsu N (November 2010). "MALAT-1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes". FEBS Letters. 584 (22): 4575–4580. doi:10.1016/j.febslet.2010.10.008. PMID 20937273. S2CID 207575862.
  6. ^ Chojnowski JL, Braun EL (Jul 15, 2012). "An unbiased approach to identify genes involved in development in a turtle with temperature-dependent sex determination". BMC Genomics. 13: 308. doi:10.1186/1471-2164-13-308. PMC 3434017. PMID 22793670.
  7. ^ Kryger R, Fan L, Wilce PA, Jaquet V (November 2012). "MALAT-1, a non protein-coding RNA is upregulated in the cerebellum, hippocampus and brain stem of human alcoholics". Alcohol. 46 (7): 629–634. doi:10.1016/j.alcohol.2012.04.002. PMID 22560368.
  8. ^ Tian X, Xu G (2015). "Clinical value of lncRNA MALAT1 as a prognostic marker in human cancer: systematic review and meta-analysis". BMJ Open. 5 (9): e008653. doi:10.1136/bmjopen-2015-008653. PMC 4593150. PMID 26423854.  
  9. ^ Wei Y, Niu B (2015). "Role of MALAT1 as a Prognostic Factor for Survival in Various Cancers: A Systematic Review of the Literature with Meta-Analysis". Disease Markers. 2015: 164635. doi:10.1155/2015/164635. PMC 4572489. PMID 26420912.  This article incorporates text from this source, which is available under the CC BY 4.0 license.

Further reading edit

External links edit