Genetic and epigenetic factors in regulation of microRNA in colorectal cancers

Vinci, Serena; Gelmini, Stefania; Mancini, Irene; Malentacchi, Francesca; Pazzagli, Mario; Beltrami, Cristina; Pinzani, Pamela; Orlando, Claudio

doi:10.1016/j.ymeth.2012.09.002

Cited by 80 publications

(73 citation statements)

References 43 publications

(57 reference statements)

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“…There were fifteen studies of caucasian descent and twenty-four studies of Asian descent. The genotype distributions in the controls of fourteen studies were not conforming to HWE (p<0.05) (Okubo et al, 2010;Akkiz et al, 2011;Ling et al, 2011;Mittal et al, 2011;Zhou et al, 2011;Xiang et al, 2012;Shan et al, 2013;Vinci et al, 2013;Wei et al, 2013;Zou and Zhao, 2013;Bansal et al, 2014;Ma et al, 2014;Omrani et al, 2014;Wang et al, 2014).…”

Section: Methodsmentioning

confidence: 99%

“…One study was excluded as it was not associated with hsa-mir-499 rs3746444 A>G (Kupcinskas et al, 2012). After further excluding two abstracts (Hu et al, 2009;Hwang et al, 2010), thirty-nine case-control studies involving 14,136 cases and 16,937 controls were selected for meta-analysis (Hu et al, 2009;Tian et al, 2009;Catucci et al, 2010;Liu et al, 2010;Okubo et al, 2010;Srivastava et al, 2010;Akkiz et al, 2011;George et al, 2011;Ling et al, 2011;Mittal et al, 2011;Vinci et al, 2011;Zhou et al, 2011;Alshatwi et al, 2012;Chu et al, 2012;Kim et al, 2012;Min et al, 2012;Xiang et al, 2012;Zhou et al, 2012;Ahn et al, 2013;Lv et al, 2013;Shan et al, 2013;Song et al, 2013;Umar et al, 2013;Vinci et al, 2013;Wei et al, 2013;Wu et al, 2013;Zou and Zhao, 2013;Bansal et al, 2014;Chu et al, 2014;Du et al, 2014;Gutierrez-Camino et al, 2014;Hasani et al, 2014;Hou et al, 2014;Hu et al, 2014;Ma et al, 2014;Omrani et al, 2014;Pu et ...…”

Section: Methodsmentioning

confidence: 99%

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Lack of Association between Hsa-Mir-499 rs3746444 Polymorphism and Cancer Risk: Meta-analysis Findings

Jiang

Chen²,

Tang³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Epidemiologic findings concerning the association between the hsa-mir-499 rs3746444 A>G polymorphism and cancer risk have yielded mixed results. We aimed to investigate the association by performing a meta-analysis of all available studies. We searched PubMed and EMBASE for studies published up to November 2014, using odds ratios (ORs) with 95% confidence intervals (CIs) to assess the strength of any association. The BenjaminiHochberg (BH) method was used to correct the p values for multiple comparisons. We included 39 studies, including 14,136 cases and 16,937 controls. The results of overall meta-analysis suggested a borderline association between hsa-mir-499 rs3746444 polymorphism and cancer susceptibility (AG+GG vs. AA: OR=1.15, 95% CI= 1.04-1.26, corrected p value=0.04). After removing studies not conforming to Hardy-Weinberg equilibrium (HWE), however, this association disappeared (AG+GG vs AA: OR=1.18, 95% CI=1.03-1.34, corrected p value=0.21). When stratified analysis by ethnicity, cancer type or HWE in controls, although some associations between hsa-mir-499 rs3746444 polymorphism and cancer susceptibility were detected, these associations no longer existed after adjustment using BH method. In conclusion, our meta-analysis suggests that hsa-mir-499 rs3746444 A>G polymorphism is not associated with risk of cancer based on current evidence. conclusive. Many meta-analyses have examined the association of the polymorphism with cancer risk and the lasted one suggested that hsa-mir-499 rs3746444 polymorphism was a risk factor for cancer development. Since the latest meta-analysis had been performed, nineteen case-control studies (Ling

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Lack of Association between Hsa-Mir-499 rs3746444 Polymorphism and Cancer Risk: Meta-analysis Findings

Jiang

Chen²,

Tang³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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“…A comparison with the adjacent normal mucosa shows higher methylation observed in primary tumors. The miR-9-1 methylation is associated with lymph node metastases 161 . In another study, miR-9-1 and -34c have significantly reduced expression, while miR-34b has also been hypermethylated along with these two microRNAs 162 .…”

Section: Impact Of Mutationsmentioning

confidence: 99%

Colorectal cancer carcinogenesis: a review of mechanisms

Tariq¹,

Ghias²

2016

Cancer Biology &Amp; Medicine

232

138

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Colorectal cancer (CRC) is the second most common cancer in women and the third most common in men globally. CRC arises from one or a combination of chromosomal instability, CpG island methylator phenotype, and microsatellite instability. Genetic instability is usually caused by aneuploidy and loss of heterozygosity. Mutations in the tumor suppressor or cell cycle genes may also lead to cellular transformation. Similarly, epigenetic and/or genetic alterations resulting in impaired cellular pathways, such as DNA repair mechanism, may lead to microsatellite instability and mutator phenotype. Non-coding RNAs, more importantly microRNAs and long non-coding RNAs have also been implicated at various CRC stages. Understanding the specific mechanisms of tumorigenesis and the underlying genetic and epigenetic traits is critical in comprehending the disease phenotype. This paper reviews these mechanisms along with the roles of various non-coding RNAs in CRCs.

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“…It is notable that the majority of the published studies to date were conducted in Asian populations whereas our study was restricted to Europeans; it is possible these variants are in linkage disequilibrium with an ethnic‐specific risk factor or that our study was underpowered to detect a modest association. Other investigators also report non‐replication of these miRNAs in CRC cohorts of European ancestry (Hezova et al, 2012; Vinci et al, 2013; Kupcinskas et al, 2014). In addition, expression levels for these miRNAs were not reported to differ in CRC across the newly described consensus molecular subtypes of CRC (Guinney et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Germline miRNA DNA variants and the risk of colorectal cancer by subtype

Lindor

Larson

DeRycke

et al. 2016

Genes Chromosomes & Cancer

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MicroRNAs (miRNAs) regulate up to one‐third of all protein‐coding genes including genes relevant to cancer. Variants within miRNAs have been reported to be associated with prognosis, survival, response to chemotherapy across cancer types, in vitro parameters of cell growth, and altered risks for development of cancer. Five miRNA variants have been reported to be associated with risk for development of colorectal cancer (CRC). In this study, we evaluated germline genetic variation in 1,123 miRNAs in 899 individuals with CRCs categorized by clinical subtypes and in 204 controls. The role of common miRNA variation in CRC was investigated using single variant and miRNA‐level association tests. Twenty‐nine miRNAs and 30 variants exhibited some marginal association with CRC in at least one subtype of CRC. Previously reported associations were not confirmed (n = 4) or could not be evaluated (n = 1). The variants noted for the CRCs with deficient mismatch repair showed little overlap with the variants noted for CRCs with proficient mismatch repair, consistent with our evolving understanding of the distinct biology underlying these two groups. © 2016 The Authors Genes, Chromosomes & Cancer Published by Wiley Periodicals, Inc.

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Genetic and epigenetic factors in regulation of microRNA in colorectal cancers

Cited by 80 publications

References 43 publications

Lack of Association between Hsa-Mir-499 rs3746444 Polymorphism and Cancer Risk: Meta-analysis Findings

Lack of Association between Hsa-Mir-499 rs3746444 Polymorphism and Cancer Risk: Meta-analysis Findings

Colorectal cancer carcinogenesis: a review of mechanisms

Germline miRNA DNA variants and the risk of colorectal cancer by subtype

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