ENST00000513868.2

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PVT1, plasmacytoma variant translocation 1 gene that has been identified as a candidate oncogene.

Annotated Information

Name

Approved symbol: PVT1

Approved name: Pvt1 oncogene

HGNC ID: HGNC:9709

Previous names: pvt-1 (murine) oncogene homolog, MYC activator; Pvt1 oncogene homolog (mouse) ; Pvt1 oncogene (non-protein coding)

Alias symbols: NCRNA00079; LINC00079; onco-lncRNA-100; MIR1204HG

Alias names: non-protein coding RNA 79[1]; long intergenic non-protein coding RNA 79; MIR1204, MIR1205, MIR1206 and MIR1207 host gene

RefSeq ID: NR_003367

LncBook ID: HSALNT0289225

Characteristics

PVT1 gene is 1957 bp long intergenic non-coding RNA and harbors nine exons (GenBank), located on human chromosome 8q24.21 telomeric to the c-Myc gene and it is frequently involved in the translocations occurring in variant Burkitt's lymphomas and murine plasmacytomas[1].

PVT1 gene contains two non canonical Myc-binding sites (E-box CACGCG) in the promoter region proximal to the transcriptional start site (−155/−95) the consensus and the surrounding sequences are conserved in the homologous mouse and rat genes[1].

Function

Schematic representation of PVT1 involvement in ECM deposition. . Hyperglycemia causes an excessive accumulation of extracellular matrix (ECM) in the glomerular mesangium which constitutes the major pathological feature of the glomerulosclerosis or glomerular fibrosis. Hyperglycemic conditions induce an increase in PVT1 expression in MC which contributes to the increase of the two main ECM components, FN1 and COL4A1, as well as the two main regulators of ECM accumulation in the glomerule, PAI-1 and TGFB1. [2].

PVT is involved in diabetic neuropathy and tumorigenesis by affecting the protein stability of the MYC proto-oncogene [1][2].

PVT1 is a downstream target of both c-Myc and N-Myc genes [1].

The E-boxes region in the PVT1 proximal promoter is important for PVT1 transcriptional regulation by Myc proteins and reveal a novel cross-talk between PVT1 and N-Myc in neuroblastoma cells [1].

PVT1 mediate the development and progression of diabetic nephropathy through mechanisms involving ECM accumulation. PVT1 knockdown significantly reduced mRNA and protein levels of the major ECM proteins, FN1 and COL4A1, and two key regulators of ECM proteins, TGFB1 and PAI-1 [2].

PVT1 modulates thyroid cancer cell proliferation by recruiting EZH2 and regulate thyroid-stimulating hormone receptor (TSHR) [3]

PVT1 regulates prostate cancer cell growth by inducing the methylation of miR-146a [4]

C-MYC and PVT1 CNG promotes a malignant phenotype of malignant pleural mesothelioma (MPM), with C-MYC CNG stimulating cell proliferation and PVT1 both stimulating proliferation and inhibiting apoptosis [5].

PVT1 promotes cell proliferation in gastric cancer by epigenetically regulating p15 and p16 [6]


Expression

PVT1 is upregulated in gastric cancer.[7]

PVT1 expression was significantly upregulated by glucose treatment in human mesangial cells [2].

PVT1 is upregulated in thyroid tissues compared with that in adjacent tissues and was up-regulated in IHH-4, FTC-133, and 8505C cell lines compared to controls [3].

PVT1 is overexpressed in prostate cancer, non small cell lung cancer (NSCLC) and hepatocellular carcinoma (HCC) [4][8][9].

PVT1 is significantly upregulated in pancreatic cancer tissues (PCT) and overexpression of PVT1 is associated with poor prognosis in pancreatic cancer patients [10][11]

Experiment Forward Reverse
PCR CAT GGT TCC ACC AGC GTT ATT C TCC TTG CGG AAA GGA TGT TGG[1]
Knockdown 5′-GCUUGGAGGCUGAGGAGUUTT-3′ 5′-AACUCCUCAGCCUCCAAGCTT-3′[3]
Quantitative PCR 5′-TGAGAACTGTCCTTACGTGACC-3′ 5′-AGAGCACCAAGACTGGCTCT-3′[3]
qRT PCR 5′-TTACAGGCGTGTGCCACAAAGC-3′ 5′-GCCTGTAATCCCAGCACGTTGA-3′[5]

Regulation

The E-boxes region in the PVT-1 proximal promoter is important for PVT-1 transcriptional regulation by Myc proteins [1].

PVT-1 transactivation by c-Myc [1].

Disease

  • Diabetic nephropathy [2]
  • Gastric cancer [6][7]
  • Malignant pleural mesothelioma (MPM) [5]
  • Non-small cell lung cancer (NSCLC) [8]
  • Pancreatic ductal adenocarcinoma (PDAC) [11]
  • Prostate cancer [4]
  • Thyroid cancer [3]

Labs working on this lncRNA

  • Dipartimento di Oncologia Sperimentale e Applicazioni Cliniche, Università di Palermo, Palermo, Italy.[1]
  • Diabetes, Cardiovascular and Metabolic Diseases Center, Translational Genomics Research Institute, Phoenix, Arizona, United States of America.[2]
  • Department of Head and Neck Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, #145 Shandong Road, Huangpu District, Shanghai 200001, China.[3]
  • Department of Pathology, Qian-fo-shan Hospital Affiliated to Shandong University, No. 16766 Jingshi Road, Jinan, Shandong 250014, China.[4]
  • Division of Hepatobiliary and Pancreatic Surgery, Department of Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University, Zhejiang 310003, P.R. China.[9]
  • Key Laboratory of Combined Multi-Organ Transplantation, Ministry of Public Health, Hangzhou, Zhejiang 310003, P.R. China.[9]
  • Department of Gastroenterology, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, Jiangsu Province, China.[7]

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 1.9 Carramusa L, Contino F, Ferro A, Minafra L, Perconti G, Giallongo A, et al. The PVT-1 oncogene is a Myc protein target that is overexpressed in transformed cells[J]. Journal of cellular physiology. 2007,213(2):511-8.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Alvarez ML & DiStefano JK. Functional characterization of the plasmacytoma variant translocation 1 gene (PVT1) in diabetic nephropathy[J]. PloS one. 2011, 6(4):e18671.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 Zhou Q, Chen J, Feng J & Wang J. Long noncoding RNA PVT1 modulates thyroid cancer cell proliferation by recruiting EZH2 and regulating thyroid-stimulating hormone receptor (TSHR)[J]. Tumor Biology. 2016, 37(3):3105-3113.
  4. ↑ 4.0 4.1 4.2 4.3 Liu Ht, Fang L, Cheng Yx & Sun Q. LncRNA PVT1 regulates prostate cancer cell growth by inducing the methylation of miR‐146a[J]. Cancer medicine. 2016, 5(12):3512-3519.
  5. ↑ 5.0 5.1 5.2 Riquelme E, Suraokar MB, Rodriguez J, Mino B, Lin HY, Rice DC et al. Frequent coamplification and cooperation between C-MYC and PVT1 oncogenes promote malignant pleural mesothelioma[J]. Journal of Thoracic Oncology. 2014, 9(7):998-1007.
  6. ↑ 6.0 6.1 Kong R, Zhang EB, Yin DD, You LH, Xu TP, Chen WM et al. Long noncoding RNA PVT1 indicates a poor prognosis of gastric cancer and promotes cell proliferation through epigenetically regulating p15 and p16[J]. Mol Cancer. 2015, 14.
  7. ↑ 7.0 7.1 7.2 Cao WJ, Wu HL, He BS, et al. Analysis of long non-coding RNA expression profiles in gastric cancer[J]. World J Gastroenterol, 2013, 19: 3658-3664.
  8. ↑ 8.0 8.1 Yang YR, Zang SZ, Zhong CL, Li YX, Zhao SS & Feng XJ. Increased expression of the lncRNA PVT1 promotes tumorigenesis in non-small cell lung cancer[J]. Int J Clin Exp Pathol. 2014, 7(10):6929-6935.
  9. ↑ 9.0 9.1 9.2 Ding CF, Yang Z, Lv Z, Du CL, Xiao H, Peng CH et al. Long non-coding RNA PVT1 is associated with tumor progression and predicts recurrence in hepatocellular carcinoma patients[J]. Oncol Lett. 2015, 9(2):955-963.
  10. ↑ Xie ZJ, Chen XL, Li JZ, Guo YW, Li HJ, Pan XM et al. Salivary HOTAIR and PVT1 as novel biomarkers for early pancreatic cancer[J]. Oncotarget. 2016, 7(18):25408-25419.
  11. ↑ 11.0 11.1 Huang C, Yu W, Wang Q, Cui H, Wang Y, Zhang L et al. Increased expression of the lncRNA PVT1 is associated with poor prognosis in pancreatic cancer patients[J]. Minerva Med. 2015, 106(3):143-149.

sequence

>gi|5820|ref|NR_003367.3| Homo sapiens Pvt1 oncogene (PVT1), long non-coding RNA

000001 CTCCGGGCAG AGCGCGTGTG GCGGCCGAGC ACATGGGCCC GCGGGCCGGG CGGGCTCGGG GCGGCCGGGA CGAGGAGGGG 000080
000081 CGACGACGAG CTGCGAGCAA AGATGTGCCC CGGGACCCCC GGCACCTTCC AGTGGATTTC CTTGCGGAAA GGATGTTGGC 000160
000161 GGTCCCTGTG ACCTGTGGAG ACACGGCCAG ATCTGCCCTC CAGCCTGATC TTTTGGCCAG AAGGAGATTA AAAAGATGCC 000240
000241 CCTCAAGATG GCTGTGCCTG TCAGCTGCAT GGAGCTTCGT TCAAGTATTT TCTGAGCCTG ATGGATTTAC AGTGATCTTC 000320
000321 AGTGGTCTGG GGAATAACGC TGGTGGAACC ATGCACTGGA ATGACACACG CCCGGCACAT TTCAGGATAC TAAAAGTGGT 000400
000401 TTTAAGGGAG GCTGTGGCTG AATGCCTCAT GGATTCTTAC AGCTTGGATG TCCATGGGGG ACGAAGGACT GCAGCTGGCT 000480
000481 GAGAGGGTTG AGATCTCTGT TTACTTAGAT CTCTGCCAAC TTCCTTTGGG TCTCCCTATG GAATGTAAGA CCCCGACTCT 000560
000561 TCCTGGTGAA GCATCTGATG CACGTTCCAT CCGGCGCTCA GCTGGGCTTG AGCTGACCAT ACTCCCTGGA GCCTTCTCCC 000640
000641 GAGGTGCGCG GGTGACCTTG GCACATACAG CCATCATGAT GGTACTTTAA GTGGAGGCTG AATCATCTCC CCTTTGAGCT 000720
000721 GCTTGGCACG TGGCTCCCTT GGTGTTCCCC TTTTACTGCC AGGACACTGA GATTTGGAGA GAGTCTCACT CTGTGGTCCA 000800
000801 GGCTGAAGTA CAGTGGCATG ATCCCAGGTC ACTGCAACCC CCACCTCCCG GGTTCAAGTG ATCCTCCTGC CTCAGCCTCC 000880
000881 CGAGTAGCTG GTATTACAGG CGTGTGCCAC AAAGCCTGGC TAAGTTTTGT ATTTTTAGTA GAGACGGGGT TTCACCATGT 000960
000961 TGGCCAGGTT GGTCTCGAAC TCCTGACCTC AAGTGATCCA CTCACTTTGG CCTTTCAACG TGCTGGGATT ACAGGCGAGA 001040
001041 GTCACCGCAC CCGGACGACT CTGACATTTT TGAAGAGTCC AGAATCCTGT TACACCTGGG ATTTAGGCAC TTTCAATCTG 001120
001121 AAAAAATACA TATCCTTTCA GCACTCTGGA CGGACTTGAG AACTGTCCTT ACGTGACCTA AAGCTGGAGT ATTTTGAGAT 001200
001201 TGGAGAATTA AGAGCCAGTC TTGGTGCTCT GTGTTCACCT GGTTCATCTG AGGAGCTGCA TCTACCCTGC CCATGCCATA 001280
001281 GATCCTGCCC TGTTTGCTTC TCCTGTTGCT GCTAGTGGAC ATGAGAAGGA CAGAATAACG GGCTCCCAGA TTCACAAGCC 001360
001361 CCACCAAGAG GATCACCCCA GGAACGCTTG GAGGCTGAGG AGTTCACTGA GGCTACTGCA TCTTGAGACT CAGGATGAAG 001440
001441 ACCCAGCTTG GGGCTGTCAA AGAGGCCTGA AGAGGCAGAA CACCCCAGAG GAGCCTGGGG CCACCACCCA GCATCACTGT 001520
001521 GGGAAAACGG CAGCAGGAAA TGTCCTCTCG CCTGCGTGCT CCACCTCGGT CCACGCCTTC CCTCCTTCTG GAAGCCTTGC 001600
001601 CTGACCACTG GCCTGCCCCT TCTATGGGAA TCACTACTGA CCTTGCAGCT TATTATAGAC TTATATGTTT TTTGCATGTC 001680
001681 TGACACCCAT GACTCCACCT GGACCTTATG GCTCCACCCA GAAGCAATTC AGCCCAACAG GAGGACAGCT TCAACCCATT 001760
001761 ACGATTTCAT CTCTGCCCCA ACCACTCAGC AGCAAGCACC TGTTACCTGT CCACCCCCAC CCCTTCCCCC AA