Analyzing large-scale samples highlights significant association between rs10411210 polymorphism and colorectal cancer

He, Dongfeng; Ma, Lihong; Feng, Rennan; Zhang, Liangcai; Jiang, Yongshuai; Zhang, Yanqiao; Liu, Guiyou

doi:10.1016/j.biopha.2015.08.023

Cited by 23 publications

(15 citation statements)

References 27 publications

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“…Arising from the transformation of colon or rectum epithelial cells, colorectal cancer (CRC) is one of the most common malignancies worldwide and causes about 694,000 deaths every year [ 1 ]. During the initiation and progression of CRC, multiple germline and somatic mutations accumulated, particular for some critical oncogenes and tumor suppressors [ 2 , 3 ]. With great advances of the understanding of CRC pathogenesis, novel therapeutic strategies have been developed and greatly improved CRC patients’ prognosis, such as the molecularly targeted agents and immunotherapy [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA HEIH Promotes Colorectal Cancer Tumorigenesis via Counteracting miR-939‒Mediated Transcriptional Repression of Bcl-xL

et al. 2018

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PurposeStudies have found that long noncoding RNA HEIH (lncRNA-HEIH) is upregulated and facilitates hepatocellular carcinoma tumor growth. However, its clinical significances, roles, and action mechanism in colorectal cancer (CRC) remains unidentified.Materials and MethodslncRNA-HEIH expression in CRC tissues and cell lines was measured by quantitative real-time polymerase chain reaction. Cell CountingKit-8, ethynyl deoxyuridine incorporation assay, terminal deoxynucleotidyl transferase dUTP nick end labeling staining, and nude mice xenografts assays were performed to investigate the roles of lncRNA-HEIH. RNA pull-down, RNA immunoprecipitation, chromatin immunoprecipitation, and luciferase reporter assays were performed to investigate the action mechanisms of lncRNA-HEIH.ResultsIn this study, we found that lncRNA-HEIH is significantly increased in CRC tissues and cell lines. lncRNA-HEIH expression is positively associated with tumor size, invasion depth, and poor prognosis of CRC patients. Enhanced expression of lncRNA-HEIH promotes CRC cell proliferation and decreases apoptosis in vitro, and promotes CRC tumor growth in vivo. Whereas knockdown of lncRNA-HEIH inhibits CRC cell proliferation and induces apoptosis in vitro, and suppresses CRC tumor growth in vivo. Mechanistically, lncRNA-HEIH physically binds to miR-939. The interaction between lncRNA-HEIH and miR-939 damages the binding between miR-939 and nuclear factor κB (NF-κB), increases the binding of NF-κB to Bcl-xL promoter, and promotes the transcription and expression of Bcl-xL. Moreover, Bcl-xL expression is positively associatedwith lncRNA-HEIH in CRC tissues. Blocking the interaction between lncRNA-HEIH and miR-939 abolishes the effects of lncRNA-HEIH on CRC tumorigenesis.ConclusionThis study demonstrated that lncRNA-HEIH promotes CRC tumorigenesis through counteracting miR-939‒mediated transcriptional repression of Bcl-xL, and suggested that lncRNA-HEIH may serve as a prognostic biomarker and therapeutic target for CRC.

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Section: Introductionmentioning

confidence: 99%

Long Noncoding RNA HEIH Promotes Colorectal Cancer Tumorigenesis via Counteracting miR-939‒Mediated Transcriptional Repression of Bcl-xL

et al. 2018

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“…Genome-wide association studies (GWAS) are considered to be new and power approaches to detect the genetic variants of human complex diseases. Recently, GWAS have been performed and reported some novel CRC susceptibility single nucleotide polymorphisms (SNPs) with genome-wide significance ( P < 5.00E-08), and these SNPs have been repliciated by meta-anaysis methods 4 5 6 7 8 9 10 11 12 13 .…”

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confidence: 99%

Colorectal cancer risk genes are functionally enriched in regulatory pathways

Cao

Han

et al. 2016

Sci Rep

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Colorectal cancer (CRC) is a common complex disease caused by the combination of genetic variants and environmental factors. Genome-wide association studies (GWAS) have been performed and reported some novel CRC susceptibility variants. However, the potential genetic mechanisms for newly identified CRC susceptibility variants are still unclear. Here, we selected 85 CRC susceptibility variants with suggestive association P < 1.00E-05 from the National Human Genome Research Institute GWAS catalog. To investigate the underlying genetic pathways where these newly identified CRC susceptibility genes are significantly enriched, we conducted a functional annotation. Using two kinds of SNP to gene mapping methods including the nearest upstream and downstream gene method and the ProxyGeneLD, we got 128 unique CRC susceptibility genes. We then conducted a pathway analysis in GO database using the corresponding 128 genes. We identified 44 GO categories, 17 of which are regulatory pathways. We believe that our results may provide further insight into the underlying genetic mechanisms for these newly identified CRC susceptibility variants.

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“…The inclusion criteria for stable COPD comprised airflow limitation as indicated by post-bronchodilator FEV1/FVC <70% and FEV1 ≤70% of normal predicted values. The severity of airflow limitation was classified according to the GOLD standard (Global Initiative for Chronic Obstructive Lung Disease) as follows: IImoderate, III-severe, and IV-very severe; (4) The control subjects were in Hardy-Weinberg equilibrium (HWE); (5) The selected studies provided SNP genotype amounts or sufficient data for calculation; and (6) The selected studies provided an odds ratio (OR) with a 95% confidence interval (CI) or sufficient data for calculation (He et al, 2015).…”

Section: Inclusion and Exclusion Criteriamentioning

confidence: 99%

Different Associations Between the IREB2 Variants and Chronic Obstructive Pulmonary Disease Susceptibility

et al. 2020

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Background: Iron responsive element binding protein 2 ( IREB2 ) variants may be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). Recently, many studies have been performed on IREB2 susceptibility variants, including rs2568494, rs2656069, rs10851906, rs12593229, and rs13180, associated with COPD. However, inconsistent findings have been reported. The aim of our research was to determine the association of IREB2 SNPs with COPD. Methods: A comprehensive meta-analysis was performed to accurately estimate the association between IREB2 variants and COPD among four different genetic models. Results: This meta-analysis included a total of 4,096 patients and 5,870 controls. Here, we investigated the 5 IREB2 variants to identify COPD risk. Our results indicate that rs2568494 was associated with an increased risk of COPD for the dominant model (AA+GA vs. GG: OR = 1.150, 95% CI: 1.5–1.304, P = 0.029); rs2656069 was associated with a decreased risk of COPD for the recessive model (GG vs. AA+AG: OR = 0.589, 95% CI: 0.440–0.789; P = 0.000), additive model (GG vs. AA: OR =0.641, 95% CI: 0.441–0.931; P = 0.020), and allele model (G vs. A: OR = 0.812, 95% CI: 0.668–0.988; P = 0.037); and rs10851906 was associated with a decreased risk of COPD for the recessive model (GG vs. AA+AG: OR = 0.732, 95% CI: 0.560–0.958; P = 0.023) and additive model (GG vs. AA: OR = 0.777, 95% CI: 0.637–0.947; P = 0.012). Conclusion: Our findings suggest that the IREB2 rs2568494 minor alleles A may be a genetic factor in susceptibility to COPD. In addition, the minor alleles G of rs2656069 and rs10851906 appear to have a protective effect.

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Analyzing large-scale samples highlights significant association between rs10411210 polymorphism and colorectal cancer

Cited by 23 publications

References 27 publications

Long Noncoding RNA HEIH Promotes Colorectal Cancer Tumorigenesis via Counteracting miR-939‒Mediated Transcriptional Repression of Bcl-xL

Long Noncoding RNA HEIH Promotes Colorectal Cancer Tumorigenesis via Counteracting miR-939‒Mediated Transcriptional Repression of Bcl-xL

Colorectal cancer risk genes are functionally enriched in regulatory pathways

Different Associations Between the IREB2 Variants and Chronic Obstructive Pulmonary Disease Susceptibility

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