GAS5

gene
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Also known as SNHG2NCRNA00030

Summary

GAS5 (growth arrest specific 5, HGNC:16355) is a long non-coding RNA gene on chromosome 1q25.1.

This gene produces a spliced long non-coding RNA and is a member of the 5’ terminal oligo-pyrimidine class of genes. It is a small nucleolar RNA host gene, containing multiple C/D box snoRNA genes in its introns. Part of the secondary RNA structure of the encoded transcript mimics glucocorticoid response element (GRE) which means it can bind to the DNA binding domain of the glucocorticoid receptor (nuclear receptor subfamily 3, group C, member 1). This action blocks the glucocorticoid receptor from being activated and thereby stops it from regulating the transcription of its target genes. This transcript is also thought to regulate the transcriptional activity of other receptors, such as androgen, progesterone and mineralocorticoid receptors, that can bind to its GRE mimic region. Multiple functions have been associated with this transcript, including cellular growth arrest and apoptosis. It has also been identified as a potential tumor suppressor, with its down-regulation associated with cancer in multiple different tissues.

Source: NCBI Gene 60674 — RefSeq curated summary.

At a glance

  • Gene type: non-coding (lncRNA) — no protein product; not a drug target. Variant/disease associations are omitted (they would be positional, from an overlapping protein-coding gene).

Identifiers

Gene identifiers

FieldValue
HGNC IDHGNC:16355
Approved symbolGAS5
Namegrowth arrest specific 5
Location1q25.1
Locus typeRNA, long non-coding
StatusApproved
AliasesSNHG2, NCRNA00030
Ensembl geneENSG00000234741
Ensembl biotypelncRNA
OMIM608280
Entrez60674
RNAcentralURS0000D5948E — lncRNA, 634 nt, 1 organism(s)

Gene structure

Transcript identifiers

Ensembl transcripts: 177 — 148 lncRNA, 29 retained_intron

ENST00000412059, ENST00000414075, ENST00000416952, ENST00000421068, ENST00000422008, ENST00000422183, ENST00000422207, ENST00000425771, ENST00000430245, ENST00000431268, ENST00000432536, ENST00000434796, ENST00000436285, ENST00000436656, ENST00000442067, ENST00000443799, ENST00000444470, ENST00000448718, ENST00000449289, ENST00000449589, ENST00000450589, ENST00000451607, ENST00000452197, ENST00000454068, ENST00000454813, ENST00000455838, ENST00000456293, ENST00000456812, ENST00000458220, ENST00000650796, ENST00000651080, ENST00000684949, ENST00000685008, ENST00000685039, ENST00000685107, ENST00000685159, ENST00000685758, ENST00000686231, ENST00000686460, ENST00000686878, ENST00000686918, ENST00000686995, ENST00000687022, ENST00000687063, ENST00000687189, ENST00000687409, ENST00000687435, ENST00000687549, ENST00000687710, ENST00000687987, ENST00000688557, ENST00000688573, ENST00000688895, ENST00000688952, ENST00000689238, ENST00000689469, ENST00000689860, ENST00000689895, ENST00000689958, ENST00000690172, ENST00000690228, ENST00000690349, ENST00000690448, ENST00000690761, ENST00000690941, ENST00000691056, ENST00000691137, ENST00000691213, ENST00000691712, ENST00000691982, ENST00000692671, ENST00000692994, ENST00000693030, ENST00000693348, ENST00000693450, ENST00000693459, ENST00000693469, ENST00000693521, ENST00000702934, ENST00000702964, ENST00000703008, ENST00000703030, ENST00000703037, ENST00000703041, ENST00000703044, ENST00000703049, ENST00000703057, ENST00000703059, ENST00000703075, ENST00000703081, ENST00000703096, ENST00000827943, ENST00000827944, ENST00000827945, ENST00000827946, ENST00000827947, ENST00000827948, ENST00000827949, ENST00000827950, ENST00000827951, ENST00000827952, ENST00000827953, ENST00000827954, ENST00000827955, ENST00000827956, ENST00000827957, ENST00000827958, ENST00000827959, ENST00000827960, ENST00000827966, ENST00000827967, ENST00000827968, ENST00000827969, ENST00000827970, ENST00000827971, ENST00000827972, ENST00000827973, ENST00000827974, ENST00000827975, ENST00000827976, ENST00000827977, ENST00000827978, ENST00000827979, ENST00000827980, ENST00000827981, ENST00000827982, ENST00000827983, ENST00000827984, ENST00000827985, ENST00000827986, ENST00000827987, ENST00000827988, ENST00000827989, ENST00000827990, ENST00000827991, ENST00000827992, ENST00000827993, ENST00000827994, ENST00000827995, ENST00000827996, ENST00000827997, ENST00000827998, ENST00000827999, ENST00000828000, ENST00000828001, ENST00000828002, ENST00000828003, ENST00000828004, ENST00000828005, ENST00000828006, ENST00000828007, ENST00000828008, ENST00000828009, ENST00000828010, ENST00000828011, ENST00000828012, ENST00000828013, ENST00000828014, ENST00000828015, ENST00000828016, ENST00000828017, ENST00000828018, ENST00000828019, ENST00000828020, ENST00000828021, ENST00000828022, ENST00000828023, ENST00000828024, ENST00000828025, ENST00000828026, ENST00000828027, ENST00000828028, ENST00000828029, ENST00000828030, ENST00000828031, ENST00000828032, ENST00000828033

RefSeq mRNA: 0 — MANE Select: None

Canonical transcript exons

ENST00000412059 — 10 exons

ExonStartEnd
ENSE00001606190173864257173864704
ENSE00001619916173866761173866796
ENSE00001654295173866177173866206
ENSE00001664078173866991173867043
ENSE00001671494173866528173866567
ENSE00001722305173865471173865547
ENSE00001725551173863895173864075
ENSE00001739773173865857173865894
ENSE00001757939173865229173865282
ENSE00004240423173867960173867996

Expression profiles

Bgee: expression breadth ubiquitous, 256 present calls, max score 99.72.

FANTOM5 (CAGE): breadth ubiquitous, TPM avg 19.1014 / max 713.7709, expressed in 1713 samples.

FANTOM5 promoters (2 alternative TSS)

Promoter IDTPM avgSamples expressed
1596619.10141713
159610.6669369

Top tissues by expression

256 total, by Bgee expression score (0-100, higher = more expressed):

TissueAnatomy IDExpression scoreQuality
left ovaryUBERON:000211999.72gold quality
body of pancreasUBERON:000115099.69gold quality
cortical plateUBERON:000534399.69gold quality
right ovaryUBERON:000211899.67gold quality
ovaryUBERON:000099299.65gold quality
cartilage tissueUBERON:000241899.65gold quality
right uterine tubeUBERON:000130299.64gold quality
endocervixUBERON:000045899.57gold quality
skin of abdomenUBERON:000141699.53gold quality
ganglionic eminenceUBERON:000402399.51gold quality
upper arm skinUBERON:000426399.50gold quality
lower esophagus mucosaUBERON:003583499.50gold quality
fallopian tubeUBERON:000388999.49gold quality
body of uterusUBERON:000985399.49gold quality
pancreasUBERON:000126499.48gold quality
ectocervixUBERON:001224999.48gold quality
mucosa of stomachUBERON:000119999.46gold quality
tibial nerveUBERON:000132399.45gold quality
oviduct epitheliumUBERON:000480499.45gold quality
skin of legUBERON:000151199.44gold quality
uterine cervixUBERON:000000299.43gold quality
stromal cell of endometriumCL:000225599.42gold quality
vaginaUBERON:000099699.42gold quality
left uterine tubeUBERON:000130399.41gold quality
islet of LangerhansUBERON:000000699.39gold quality
body of stomachUBERON:000116199.39gold quality
zone of skinUBERON:000001499.36gold quality
minor salivary glandUBERON:000183099.36gold quality
lymph nodeUBERON:000002999.35gold quality
right lungUBERON:000216799.30gold quality

Single-cell (SCXA)

Detected in 2 experiment(s), a significant marker in 1.

ExperimentMarker?Max mean expression
E-MTAB-10596no1133.62
E-ANND-3no0.00

Regulation

Is transcription factor: no

Literature-anchored findings (GeneRIF, showing 40)

  • Growth arrest-specific transcript 5 gene fuses to BCL6 as a result of t(1;3)(q25;q27) in a patient with B-cell lymphoma (PMID:18406879)
  • GAS5 transcript levels were significantly reduced in breast cancer samples relative to adjacent unaffected normal breast epithelial tissues. (PMID:18836484)
  • Data show that that Gas5 is a “riborepressor” of the GR, influencing cell survival and metabolic activities during starvation by modulating the transcriptional activity of the GR. (PMID:20124551)
  • Critical role for non-coding RNA GAS5 in growth arrest and rapamycin inhibition in human T-lymphocytes. (PMID:21428924)
  • we found that the RNA degradation pathway can regulate the function of the GAS5 ncRNA in mammalian cells. (PMID:23383264)
  • a decrease in GAS5 expression is associated with Renal cell carcinoma genesis and progression and overexpression of GAS5 can act as a tumor suppressor for Renal cell carcinoma (PMID:23621190)
  • GAS5 promotes the apoptosis of prostate cells, and exonic sequence, i.e. GAS5 lncRNA, is sufficient to mediate this activity (PMID:23676682)
  • Authors identify miR-21 in this GAS5-RISC complex, implying that miR-21 and GAS5 may regulate each other in a way similar to the microRNA-mediated silencing of target mRNAs. (PMID:23933812)
  • Data suggest an important role of gas5 in the molecular etiology of pancreatic cancer. (PMID:24026436)
  • Downregulation of GAS5 promotes bladder cancer cell proliferation, partly by regulating CDK6. (PMID:24069260)
  • This report further demonstrates the critical role played by GAS5 in the growth arrest of mammalian cells (PMID:24319682)
  • GAS5 could serve as a potential diagnostic marker for NSCLC and may be a novel therapeutic target in patients with NSCLC (PMID:24357161)
  • Regulation of apoptosis by long non-coding RNA GAS5 in breast cancer cells (PMID:24789445)
  • GAS5 is significantly downregulated in gastric cancer tissues and may represent a new marker of poor prognosis and a potential therapeutic target for gastric cancer intervention. (PMID:24884417)
  • GAS5 levels modify cell proliferation in vitro; GAS5 expression in malignant pleural mesothelioma tissue is associated with cell quiescence and podoplanin expression. (PMID:24885398)
  • Data suggest that the GAS5-derived snoRNAs are under control of p53 and that they have an important role in mediating the p53 response to DNA damage, which may not relate to their function in the ribosome. (PMID:24926850)
  • Our results indicated that GAS5 expression was an independent prognostic factor for patients with liver cancer (PMID:25120813)
  • GAS5, plays a critical role in the regulation of miR-21 during osteoarthritis. (PMID:25196583)
  • Suggest that lncRNA GAS5 is a novel molecule involved in cervical cancer progression, which provide a potential prognostic biomarker and therapeutic target. (PMID:25400758)
  • Subjects being poor responders to GCs presented higher levels of GAS5 and NR3C1 in comparison with good responders (PMID:25601472)
  • Pro-inflammatory mediators up-regulate GAS5 levels in both airway epithelial and smooth muscle cells, and that decreasing GAS5 levels can enhance glucocorticoid action in airway epithelial cells. (PMID:25615620)
  • mTOR inhibition enhances GAS5 transcript levels in certain prostate cancer cell lines. This selectivity is likely to be related to endogenous GAS5 expression levels, since GAS5 lncRNA is itself required for mTOR inhibitor action in prostate cancer cells. (PMID:25650269)
  • demonstrate that a piRNA derived from Growth Arrest Specific 5, a tumor-suppressive long non-coding RNA, potently upregulates the transcription of tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), a proapoptotic protein (PMID:25779046)
  • our results indicated that GAS5 LncRNA may represent a potential biomarker for the diagnosis of lung adenocarcinoma and that GAS5 might play a novel role in the development of the resistance to gefitinib (PMID:25925741)
  • Long non-coding RNA GAS5 down-regulation reduced the YBX1 protein level, which decreased YBX1-transactivated p21 expression and abolished G1 phase cell cycle arrest in stomach cancer. (PMID:25959498)
  • our findings provided evidence that rs145204276 may contribute to hepatocarcinogenesis by affecting methylation status of the GAS5 promoter and subsequently its transcriptional activity and serving as a potential therapy target for hepatocelluar carcinoma (PMID:26163879)
  • These data enhance our understanding of the important role that GAS5 plays in the molecular etiology of GC and suggest a potential of GAS5 as a new therapeutic target for GC treatment. (PMID:26278580)
  • Gas5 suppresses tumor malignancy by downregulating miR-222 (PMID:26370254)
  • GAS5 acts as a tumor suppressor in HCCs. (PMID:26404135)
  • identified GAS5 as a target of microRNA-222 (miR-222) and showed that miR-222 could inhibit the expression of GAS5. Interestingly, GAS5 could also repress miR-222 expression (PMID:26446789)
  • the findings of the present study revealed that GAS5 is downregulated in EOC specimens, and GAS5 inhibits EOC cell proliferation, migration and invasion, and promotes cell apoptosis (PMID:26503132)
  • GAS5 acts as an tumor suppressor lncRNA in endometrial cancer. Through inhibiting the expression of miR-103, GAS5 significantly enhanced the expression of PTEN to promote cancer cell apoptosis (PMID:26511107)
  • The results of the present study demonstrated that GAS5 was able to suppress bladder cancer cell proliferation, at least partially, by suppressing the expression of CCL1. (PMID:26548923)
  • In this review, we will summarize the current knowledge about LncRNA GAS5, a recently identified tumor suppressor involved in several cancers, like breast cancer, prostate cancer, lung cancer, and colorectal cancer (PMID:26634743)
  • Plasma lncRNA GAS5 may have the potential to assess the surgical effects and prognosis for BC patients. (PMID:26662314)
  • the present study suggests an important role of GAS5 in the molecular etiology of Hepatocellular carcinoma (HCC) and suggests the potential application of GAS5 in HCC therapy (PMID:26707238)
  • GAS5 long non-coding RNA, human, may potentially serve as a novel biomarker for cancer metastasis and prognosis. (PMID:26763654)
  • Study shows that GAS5 may function as a tumor suppressor by inhibiting melanoma cell invasiveness via the regulation of MMP2 expression and its activity. (PMID:26846479)
  • Data show that the hormone response element mimic (HREM) oligonucleotide could overcome apoptosis resistance secondary to deficient endogenous Growth arrest-specific 5 long non-coding RNA (GAS5 lncRNA) levels. (PMID:26862727)
  • Long non-coding RNA GAS5 inhibited hepatitis C virus replication by binding viral NS3 protein. (PMID:26945984)

Cross-species orthologs

0 orthologs

Protein

Non-coding RNA — no protein product; not a drug target.

Function

No curated pathway, Gene-Ontology, or interaction data.

Disease & clinical

No curated disease, variant, or cancer-driver associations.

Drugs & pharmacology

No drug or pharmacology data — not an established drug target.

No linked Atlas pages yet — the cross-entity mesh grows as the corpus expands.