Integrative Analysis of Normal Long Intergenic Non-Coding RNAs in Prostate Cancer

Bawa, Pushpinder; Zackaria, Sajna; Verma, Mohit; Gupta, Saurabh; Raghunathan, Srivatsan; Chaudhary, Bibha; Srinivasan, Subhashini

doi:10.1371/journal.pone.0122143

Cited by 28 publications

(30 citation statements)

References 35 publications

(41 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…POU5F1B promotes gastric cancer [48] and hepatocellular carcinoma ( Table 1) [49]. Prostate Cancer-Associated Transcript 1 (PCAT1) and PCAT2 are upregulated in PC [50][51][52]. PCAT1 also promotes ovarian cancer cell proliferation [53] and is associated with poor prognosis in colorectal cancer (CRC) ( Table 1) [54].…”

Section: Association Of the 8q2421 Gene Desert With Oncogenesismentioning

confidence: 99%

The Oncogenic Potential of the Centromeric Border Protein FAM84B of the 8q24.21 Gene Desert

Lin

Kapoor

et al. 2020

Genes

View full text Add to dashboard Cite

FAM84B is a risk gene in breast and prostate cancers. Its upregulation is associated with poor prognosis of prostate cancer, breast cancer, and esophageal squamous cell carcinoma. FAM84B facilitates cancer cell proliferation and invasion in vitro, and xenograft growth in vivo. The FAM84B and Myc genes border a 1.2 Mb gene desert at 8q24.21. Co-amplification of both occurs in 20 cancer types. Mice deficient of a 430 Kb fragment within the 1.2 Mb gene desert have downregulated FAM84B and Myc expressions concurrent with reduced breast cancer growth. Intriguingly, Myc works in partnership with other oncogenes, including Ras. FAM84B shares similarities with the H-Ras-like suppressor (HRASLS) family over their typical LRAT (lecithin:retinal acyltransferase) domain. This domain contains a catalytic triad, H23, H35, and C113, which constitutes the phospholipase A 1/2 and O-acyltransferase activities of HRASLS1-5. These enzymatic activities underlie their suppression of Ras. FAM84B conserves H23 and H35 but not C113 with both histidine residues residing within a highly conserved motif that FAM84B shares with HRASLS1-5. Deletion of this motif abolishes FAM84B oncogenic activities. These properties suggest a collaboration of FAM84B with Myc, consistent with the role of the gene desert in strengthening Myc functions. Here, we will discuss recent research on FAM84B-derived oncogenic potential.Genes 2020, 11, 312 2 of 15 non-coding RNA (lnRNA), and on its upstream or centromeric side sits a 1.2 Mb gene desert with the centromeric side bordered by the FAM84B or LRATD2 gene ( Figure 1). The unique feature of this gene desert is the existence of multiple (lnRNAs) (PCAT1, PCAT2, POU5F1B, CCAT1, CCAT2, CASC8, CASC11, CASC19, and CASC21) with FAM84B and Myc being the only protein coding genes (Figure 1) [12][13][14]. In view of Myc being the most-well-studied oncogene and the 8q24 gene desert as a region that is frequently amplified in cancer, FAM84B stands as a promising target for oncogenic activities; nonetheless, its impact on tumorigenesis remained unknown until recently. As the oncogenic potential of the non-coding RNAs of PVT1 and those within the gene desert (Figure 1) has been recently reviewed [13][14][15][16][17], we will focus on the emerging role of FAM84B in tumorigenesis in this review. We will briefly discuss the 8q24 gene desert with respect to oncogenesis to set the stage for the following systemic examination of the evidence pertinent to FAM84B-derived tumorigenesis. The main materials used in this review were chosen based on the PRISMA (preferred reporting items for systematic reviews and meta-analyses) Guidelines [18,19]. A literature search of the PubMed database for (1) "8q24 gene desert", revealed 28 papers with 6 irrelevant to tumorigenesis (Figure 2A) and (2) "FAM84B", identified 21 articles, including non-English papers (n = 1) and articles not directly related to FAM84B and cancer (n = 2) ( Figure 2B). After excluding these items, 22 articles on 8q24 gene desert and 18 papers related to the FAM84B topic h...

show abstract

Section: Association Of the 8q2421 Gene Desert With Oncogenesismentioning

confidence: 99%

The Oncogenic Potential of the Centromeric Border Protein FAM84B of the 8q24.21 Gene Desert

Lin

Kapoor

et al. 2020

Genes

View full text Add to dashboard Cite

show abstract

“…Causative genes at this locus are unknown. Although several long intergenic noncoding RNAs at this locus may be up-regulated in prostate cancer (64), much emphasis has remained on this region regulating protein-coding genes (e.g., refs. 65,66).…”

Section: −25mentioning

confidence: 99%

Structural variants caused byAluinsertions are associated with risks for many human diseases

Payer

Steranka

Yang

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

126

102

View full text Add to dashboard Cite

Interspersed repeat sequences comprise much of our DNA, although their functional effects are poorly understood. The most commonly occurring repeat is the Alu short interspersed element. New Alu insertions occur in human populations, and have been responsible for several instances of genetic disease. In this study, we sought to determine if there are instances of polymorphic Alu insertion variants that function in a common variant, common disease paradigm. We cataloged 809 polymorphic Alu elements mapping to 1,159 loci implicated in disease risk by genome-wide association study (GWAS) (P < 10−8). We found that Alu insertion variants occur disproportionately at GWAS loci (P = 0.013). Moreover, we identified 44 of these Alu elements in linkage disequilibrium (r2 > 0.7) with the trait-associated SNP. This figure represents a >20-fold increase in the number of polymorphic Alu elements associated with human phenotypes. This work provides a broader perspective on how structural variants in repetitive DNAs may contribute to human disease.

show abstract

“…The MYC oncogene works as a transcriptional activator that is involved in cell growth, apoptosis, and differentiation (8,(18)(19)(20)(21)(22). CASC11, another neighboring gene of PVT1, is also reported to be differentially upregulated in prostate cancer compared with normal prostate (23). In addition, SNPs in the CASC11-MYC-PVT1 region in the chromosome 8q24.21 ( Fig.…”

Section: Introductionmentioning

confidence: 99%

Interactions ofPVT1andCASC11on Prostate Cancer Risk in African Americans

Lin

Callan

Fang

et al. 2019

Cancer Epidemiology, Biomarkers &Amp; Prevention

View full text Add to dashboard Cite

Background: African American (AA) men have a higher risk of developing prostate cancer than white men. SNPs are known to play an important role in developing prostate cancer. The impact of PVT1 and its neighborhood genes (CASC11 and MYC) on prostate cancer risk are getting more attention recently. The interactions among these three genes associated with prostate cancer risk are understudied, especially for AA men. The objective of this study is to investigate SNP-SNP interactions in the CASC11-MYC-PVT1 region associated with prostate cancer risk in AA men.Methods: We evaluated 205 SNPs using the 2,253 prostate cancer patients and 2,423 controls and applied multiphase (discovery-validation) design. In addition to SNP individual effects, SNP-SNP interactions were evaluated using the SNP Interaction Pattern Identifier, which assesses 45 patterns.Results: Three SNPs (rs9642880, rs16902359, and rs12680047) and 79 SNP-SNP pairs were significantly associated with prostate cancer risk. These two SNPs (rs16902359 and rs9642880) in CASC11 interacted frequently with other SNPs with 56 and 9 pairs, respectively. We identified the novel interaction of CASC11-PVT1, which is the most common gene interaction (70%) in the top 79 pairs. Several top SNP interactions have a moderate to large effect size (OR, 0.27-0.68) and have a higher prediction power to prostate cancer risk than SNP individual effects.Conclusions: Novel SNP-SNP interactions in the CASC11-MYC-PVT1 region have a larger impact than SNP individual effects on prostate cancer risk in AA men.Impact: This gene-gene interaction between CASC11 and PVT1 can provide valuable information to reveal potential biological mechanisms of prostate cancer development. reverse-reverse coding for SNP1 and SNP2. "AA_int" pattern means a monotonic risk (OR > 1) or protective (OR < 1) effect based on the selected alleles. See Supplementary Tables S2 and S3 for details. Lin et al. Acquisition of data (provided animals, acquired and managed patients, provided facilities, etc.): H.-Y. Lin, H.-Y. Tung Analysis and interpretation of data (e.g., statistical analysis, biostatistics, computational analysis):

show abstract

Integrative Analysis of Normal Long Intergenic Non-Coding RNAs in Prostate Cancer

Cited by 28 publications

References 35 publications

The Oncogenic Potential of the Centromeric Border Protein FAM84B of the 8q24.21 Gene Desert

The Oncogenic Potential of the Centromeric Border Protein FAM84B of the 8q24.21 Gene Desert

Structural variants caused byAluinsertions are associated with risks for many human diseases

Interactions ofPVT1andCASC11on Prostate Cancer Risk in African Americans

Contact Info

Product

Resources

About