Difference between revisions of "NONHSAT076153"

From LncRNAWiki
Jump to: navigation, search
Line 6: Line 6:
  
 
===Characteristics===
 
===Characteristics===
−
''PCGEM1'' is located at human chromosome 2q32.3 (HGNC), consists of three exons that comprehends 1603 bp (GenBank).
+
''PCGEM1'' is located at human chromosome 2q32.3 (HGNC), consists of three exons that comprehends 1603 bp (GenBank) <ref name="ref8" />.
  
 
===Function===
 
===Function===
Line 90: Line 90:
 
<ref name="ref7"> Hung C L, Wang L Y, Yu Y L, et al. A long noncoding RNA connects c-Myc to tumor metabolism[J]. Proceedings of the National Academy of Sciences. 2014, 111(52):18697-18702.
 
<ref name="ref7"> Hung C L, Wang L Y, Yu Y L, et al. A long noncoding RNA connects c-Myc to tumor metabolism[J]. Proceedings of the National Academy of Sciences. 2014, 111(52):18697-18702.
 
</ref>(7)
 
</ref>(7)
 +
<ref name="ref8"> Srikantan V, Zou Z, Petrovics G, et al. PCGEM1, a prostate-specific gene, is overexpressed in prostate cancer[J]. Proceedings of the National Academy of Sciences. 2000, 97(22): 12216-12221.
 +
</ref>(8)
 
</references>
 
</references>
  

Revision as of 08:42, 14 November 2018

PCGEM1 (Prostate cancer gene expression marker 1) is a long non-coding RNA (lncRNA) overexpressed in prostate cancer (PCa) cells that promotes PCa initiation and progression and protects against chemotherapy-induced apoptosis [1]. PCGEM1 has been characterised as a high-risk PCa marker and a potential biomarker for neoplasms responsive to chemoprevention by phytosterols [2].

Annotated Information

Name

PCGEM1: Prostate-specific transcript, LINC00071 (HGNC)

Characteristics

PCGEM1 is located at human chromosome 2q32.3 (HGNC), consists of three exons that comprehends 1603 bp (GenBank) [3].

Function

PCGEM1 regulates expression of metabolic enzymes in multiple pathways.Expression of the metabolic genes in PCGEM1 knockdown LNCaP cell was examined by qRT-PCR. Positive and negative values indicate up and down-regulation compared with control cell, respectively.[4]

PCGEM1 regulates prostate cancer cell growth and tumor metabolism [4][1][2]. PCGEM1 regulates metabolism at a transcriptional level that affects multiple metabolic pathways, including glucose and glutamine metabolism, the pentose phosphate pathway, nucleotide and fatty acid biosynthesis, and the tricarboxylic acid cycle. The PCGEM1-mediated gene regulation takes place in part through AR activation, but predominantly through c-Myc activation, regardless of hormone or AR status. PCGEM1 binds directly to target promoters, physically interacts with c-Myc, promotes chromatin recruitment of c-Myc, and enhances its transactivation activity [4].

Over-expression of PCGEM1 leads to inhibition of apoptosis induced by doxorubicin [5]. PCGEM1 and PRNCR1 interact with the androgen receptor (AR) bound at DNA-enhancer regions in a ligand-dependent fashion and facilitate the chromosomal looping between AR-bound enhancers and the promoter sequences of androgen-responsive genes [2].

Reciprocal regulation of PCGEM1 and miR-145 promote proliferation of LNCaP prostate cancer cells and nu/nu PCa tumor growth. Both downregulation of a tumor-promoting long noncoding RNA PCGEM1 or overexpression of the tumor suppressor miR-145 reduced the proliferation and invasive capacity of prostate cancer cells in vitro and in vivo [1].

Disease

prostate cancer

Expression

PCGEM1, was expressed exclusively in human prostate tissue, was dramatically upregulated in PCa tissues compared with normal prostate tissues. Prostate tissue-specific and prostate cancer-associated (Srikantan 2000). Cholesterols upregulate the expression of PCGEM1 even in androgen-insensitive prostate cancer cell lines while phytosterols reverse this effect (Ifere 2009). PCGEM1 overexpression in LNCaP and in NIH3T3 cells promotes cell proliferation and a dramatic increase in colony formation, suggesting a biological role of PCGEM1 in cell growth regulation (Petrovics 2004). Low specificity as a biomarker for prostate cancer (14%) (Bialkowska-Hobrzanska 2006).

Experiment Forward primer Reverse primer
Quantitative PCR 5′-TGCCTCAGCCTCCCAAGTAAC-3′ 5′-GGCCAAAATAAAACCAAACAT-3′[6]
siRNA 5′-GCCCUACCUAUGAUUUCAUAU-3′ 5′-AUAUGAAAUCAUAGGUAGGGC-3′[1]
qRT-PCR 5′-CACGTGGAGGACTAAGGGTA-3′ 5′-TTGCAACAAGGGCATTTCAG-3′[1]

Regulation

p54/nrb-mediated regulation of PCGEM1[7]

p54/nrb interact with the PCGEM1 promoter and regulate PCGEM1 [7].

Allelic Information and Variation

PCGEM1 polymorphisms may contribute to PCa risk in Chinese men. Men carrying single nucleotide polymorphisms (SNPs) of PCGEM1, i.e. rs6434568 AC and rs16834898 AC, had a lower PCa risk in comparison to the ones harboring CC and AA genotypes, respectively [8].

Labs working on this lncRNA

  • Howard Hughes Medical Institute, Department of Medicine, University of California San Diego, La Jolla, California 92093, USA.
  • Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
  • Department of Urology, School of Medicine, University of California Davis, Sacramento, California 95817, USA.
  • Graduate Program, Kellogg School of Science and Technology, The Scripps Research Institute, La Jolla, California 92037, USA.
  • Bioinformatics and System Biology Program, Department of Bioengineering, University of California San Diego, La Jolla, California 92093, USA.
  • Neurosciences Graduate Program, Department of Biological Sciences, University of California San Diego, La Jolla, California 92093, USA.
  • State Key Laboratory of Reproductive Medicine, Institute of Toxicology, Nanjing Medical University, Nanjing, China.[8]
  • Department of Environmental Genomics, Jiangsu Key Laboratory of Cancer Biomarkers, Prevention and Treatment, Cancer Center, Nanjing Medical University, Nanjing, China.[8]
  • Department of Genetic Toxicology, Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing, China.[8]
  • Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.[8]
  • Department of Environmental Genomics, School of Public Health, Nanjing Medical University, 818 East Tianyuan Road, Nanjing, Jiangsu 211166, China. [8]
  • Department of Laboratory, Central Hospital of Panyu District, 8 Fuyu Dong Road, shiqiao, Guangzhou, Guangdong 511400, P R China.[1]
  • The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou 510620, China.[1]
  • Department of Pharmacology and Toxicology, Cancer Institute, University of Mississippi Medical Center, Jackson, MS, USA.[7]
  • Department of Radiation Oncology, University of Mississippi Medical Center, Jackson, MS, USA.[7]
  • Department of Biochemistry, Cancer Institute, University of Mississippi Medical Center, Jackson, MS, USA.[7]
  • Department of Radiation Oncology, Duke University Medical Center, Durham, NC, USA.[7]
  • System Biosciences, Mountain View, CA, USA.[7]
  • Department of Pulmonary Medicine, Tongji Hospital, Tongji University, Shanghai, China.[7]
  • Department of Pathology, University of Mississippi Medical Center, Jackson, MS, USA.[7]
  • College of Life Sciences, Zhejiang Sci-Tech University, Hangzhou, China.[7]
  • Department of Biochemistry and Molecular Medicine, Comprehensive Cancer Center, University of California at Davis, Sacramento, CA 95817.[4]
  • Institute of Molecular and Genomic Medicine, National Health Research Institutes, Zhunan Town, Miaoli County 350, Taiwan.[4]
  • Department of Surgery, Center for Prostate Disease Research, Uniformed Services University of the Health Sciences, Bethesda, MD 20814-4799.[4]

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 He J H, Zhang J, Han Z P, et al. Reciprocal regulation of PCGEM1 and miR-145 promote proliferation of LNCaP prostate cancer cells[J]. Journal of Experimental & Clinical Cancer Research. 2014, 33(1):72.
  2. ↑ 2.0 2.1 2.2 Martens-Uzunova ES, Böttcher R, Croce CM, Jenster G, Visakorpi T & Calin GA. Long Noncoding RNA in Prostate, Bladder, and Kidney Cancer[J]. European Urology. 2014, 65(6):1140-1151.
  3. ↑ Srikantan V, Zou Z, Petrovics G, et al. PCGEM1, a prostate-specific gene, is overexpressed in prostate cancer[J]. Proceedings of the National Academy of Sciences. 2000, 97(22): 12216-12221.
  4. ↑ 4.0 4.1 4.2 4.3 4.4 4.5 Hung C L, Wang L Y, Yu Y L, et al. A long noncoding RNA connects c-Myc to tumor metabolism[J]. Proceedings of the National Academy of Sciences. 2014, 111(52):18697-18702.
  5. ↑ Fu X, Ravindranath L, Tran N, Petrovics G & Srivastava S. Regulation of apoptosis by a prostate-specific and prostate cancer-associated noncoding gene, PCGEM1[J]. DNA and cell biology. 2006, 25(3):135-141.
  6. ↑ Srikantan V, Zou Z, Petrovics G, et al. PCGEM1, a prostate-specific gene, is overexpressed in prostate cancer[J]. Proceedings of the National Academy of Sciences. 2000, 97(22):12216-12221.
  7. ↑ 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.8 7.9 Ho T T, Huang J, Zhou N, et al. Regulation of PCGEM1 by p54/nrb in prostate cancer[J]. Scientific reports, 2016, 6: 34529.
  8. ↑ 8.0 8.1 8.2 8.3 8.4 8.5 Xue Y, Wang M, Kang M, et al. Association between lncrna PCGEM1 polymorphisms and prostate cancer risk[J]. Prostate cancer and prostatic diseases. 2013, 16(2):139.

Basic Information

Transcript ID

NONHSAT076153

Source

NONCODE4.0

Same with

,

Classification

intergenic

Length

1603 nt

Genomic location

chr2+:193614571..193641625

Exon number

3

Exons

193614571..193614754,193615515..193615598,193640304..193641625

Genome context

Sequence

>gi

[back to top]
Retrieved from "https://ngdc.cncb.ac.cn/lncrnawiki1/index.php?title=NONHSAT076153&oldid=1275278"