Prostate cancer risk SNP rs10993994 is a trans-eQTL for SNHG11 mediated through MSMB

Bicak, Mesude; Wang, Xing; Gao, Xiaoping; Xu, Xianghua; Väänänen, Riina Minna; Taimen, Pekka; Lilja, Hans; Pettersson, Kim; Klein, Robert J.

doi:10.1093/hmg/ddaa026

Cited by 10 publications

(7 citation statements)

References 50 publications

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“…Hence, in the present study the aim was to explore the detailed mechanism by which lncRNAs regulate TNBC proliferation and migration. Previously, it has been revealed that small nucleolar RNA host gene 11 (SNHG11) acted as a tumor promoter in lung ( 15 ), prostate ( 16 ) and liver cancer ( 17 ), but it has not been studied in TNBC. Therefore, the present study mainly investigated the role and regulatory mode of SNHG11 in TNBC.…”

Section: Introductionmentioning

confidence: 99%

LncRNA SNHG11 aggravates cell proliferation and migration in triple‑negative breast cancer via sponging miR‑2355‑5p and targeting CBX5

Zhang

Wang

et al. 2021

Exp Ther Med

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Triple-negative breast cancer (TNBC) is one of the most common malignances worldwide. Concurrently, the incidence of TNBC has continued to rise in recent years. It is reported that long non-coding RNAs (lncRNAs) are involved in biological processes in numerous cancers including TNBC. Small nucleolar RNA host gene 11 (SNHG11) has already been studied and reported in some cancers. However, the role of SNHG11 in TNBC remains unknown. RT-qPCR was used to measure gene expression in the current study. CCK-8, colony formation, flow cytometry, Transwell and western blotting experiments were also performed to determine the biological function of SNHG11 in TNBC cells. Luciferase reporter and RIP assays were performed to measure relationship between genes. In the present study, the results indicated SNHG11 was highly expressed in TNBC tissues and cell lines. Moreover, SNHG11 aggravated cell proliferation and migration, and whereas it attenuated cell apoptosis in TNBC. Furthermore, SNHG11 sponged microRNA 2355-5p (miR-2355-5p) in TNBC. Silencing SNHG11 increased miR-2355-5p expression. In addition, chromobox 5 (CBX5) was identified to be targeted by miR-2355-5p in TNBC. It was also suggested that CBX5 silencing suppressed cell proliferation and migration. Furthermore, overexpressed CBX5 recovered the inhibitive influence of SNHG11 silencing on proliferative and migrative abilities of TNBC cells. Overall, SNHG11 acted as a tumor promoter in TNBC and regulated TNBC cell growth by modulating the miR-2355-5p/CBX5 axis, which indicated that it may be used as a biomarker for TNBC treatment.

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Section: Introductionmentioning

confidence: 99%

LncRNA SNHG11 aggravates cell proliferation and migration in triple‑negative breast cancer via sponging miR‑2355‑5p and targeting CBX5

Zhang

Wang

et al. 2021

Exp Ther Med

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“…For cis ‐eQTL analysis, we performed a meta‐analysis of our own linked genotype/gene expression data from prostate tissue with two data sets from dbGAP: a cohort of 470 prostate samples from dbGaP (phs000985.v1.p1) 27 and 752 samples from the Genotype‐Tissue Expression Project (GTEx) (phs000424.v7.p2) 28 . Details of our meta‐analysis approach are described elsewhere 29 . For each SNP, cis‐genes within 10 6 base pairs were taken for analysis.…”

Section: Methodsmentioning

confidence: 99%

“…28 Details of our metaanalysis approach are described elsewhere. 29 For each SNP, cisgenes within 10 6 base pairs were taken for analysis. Each SNP was showed a significant (p < 1 × 10 −4 ) interaction term between SNP and age when regressed against log PSA, and were chosen to test in the validation cohort ( Figure 2).…”

Section: Cis-eqtl Meta-analysismentioning

confidence: 99%

Genome‐wide association study identifies novel single nucleotide polymorphisms having age‐specific effect on prostate‐specific antigen levels

Bicak

Sjoberg

et al. 2020

The Prostate

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Background: Testing for prostate-specific antigen (PSA) levels in blood are widely used and associated with prostate cancer risk and outcome. After puberty, PSA levels increase by age and multiple single nucleotide polymorphisms (SNPs) have been found to be associated with PSA levels. However, the relationship between the effects of SNPs and age on PSA remains unknown. Methods: To test for SNP × age interaction, we conducted a genome-wide association study using 2394 men without prostate cancer diagnosis from Malmö, Sweden as a discovery set and 2137 men from the eMERGE study (USA) for validation. Linear regression was used to identify significant interactions between SNP and age (p < 1 × 10 −4 for discovery, p < .05 for validation). Results: The 15 SNPs from three different loci (8p11.22, 8p12, 3q25.31) are found to have age-specific effect on PSA levels. Expression quantitative trait loci (eQTLs) analysis shows that 12 SNPs from 3q25.31 locus affect the expression level of three genes: KCNAB1, SLC33A1, PLCH1. Conclusions: Our results suggest that SNPs may have age-specific effect on PSA levels, which provides new direction to study genetic markers for PSA.

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“…The rationale underlies eQTL is that germline variations alter the transcription abundances of mRNA or other transcripts to cause phenotypic changes in the cell. Many studies demonstrated that eQTL can further affect a wider spectrum of transcripts by targeting at genes with trans ‐acting regulatory activities 5,6 . Several large data consortia have been established by eQTL mapping based on large parallel sequencing projects.…”

Section: Introductionmentioning

confidence: 99%

MiR‐3130‐5p is an intermediate modulator of 2q33 and influences the invasiveness of lung adenocarcinoma by targeting NDUFS1

et al. 2021

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Genome‐wide association studies (GWAS) have reported a handful of loci associated with lung cancer risk, of which the pathogenic pathways are largely unknown. We performed cis‐expression quantitative trait loci (eQTL) mapping for 376 lung cancer related GWAS loci in 227 TCGA lung adenocarcinoma (LUAD) and reported two risk loci as eQTL of miRNA. Among the miRNAs in association with lung cancer risk, we further predicted and validated miR‐3130‐5p as an intermediate modulator of risk loci 2q33 and the tumor suppressor NDUFS1. We assessed the phenotypic impacts of the interaction between miR‐3130‐5p and NDUFS1 in both lung cancer cell lines and mice xenograft models. As a result, miR‐3130‐5p directly regulates the expression of NDUFS1 and the corresponding tumor invasiveness, migration and epithelial‐mesenchymal transition (EMT). Our findings provide important clues for the pathogenic mechanism of 2q33 in lung carcinogenesis which informs clinical diagnosis and prognosis of LUAD. We performed a cis‐eQTL analysis for 376 lung cancer risk loci based on the expression profiles of 251 miRNAs in a cohort of 227 TCGA lung adenocarcinoma. We report a novel pathogenic pathway of 2q33 via miR‐3130‐5p and NDUFS1.

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Prostate cancer risk SNP rs10993994 is a trans-eQTL for SNHG11 mediated through MSMB

Cited by 10 publications

References 50 publications

LncRNA SNHG11 aggravates cell proliferation and migration in triple‑negative breast cancer via sponging miR‑2355‑5p and targeting CBX5

LncRNA SNHG11 aggravates cell proliferation and migration in triple‑negative breast cancer via sponging miR‑2355‑5p and targeting CBX5

Genome‐wide association study identifies novel single nucleotide polymorphisms having age‐specific effect on prostate‐specific antigen levels

MiR‐3130‐5p is an intermediate modulator of 2q33 and influences the invasiveness of lung adenocarcinoma by targeting NDUFS1

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