Three common functional polymorphisms in microRNA encoding genes in the susceptibility to hepatocellular carcinoma: A systematic review and meta-analysis

Xu, Youyong; Liu, Liwen; Xiang, Xiaogang; Wang, Hui; Cai, Wei; Xie, Jiansheng; Yan, Han; Bao, Shishan; Xie, Qing

doi:10.1016/j.gene.2013.05.085

Cited by 52 publications

(49 citation statements)

References 37 publications

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“…Possibly because of the same reason of Wang's, their study showed no significant association. The meta-analysis of Xu et al 2013 [50] revealed the miR-146a C variant was associated with a decreased HCC risk and it was consistent with ours. Their study only comprised a total of ten case-control studies involving 3437 cases and 3437 controls.…”

Section: Discussionsupporting

confidence: 87%

Association between Two Common Polymorphisms and Risk of Hepatocellular Carcinoma: Evidence from an Updated Meta-Analysis

Wang

Zhang

Shi

et al. 2014

BioMed Research International

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Background. Recent studies suggested that two common polymorphisms, miR-146a G>C and miR-196a2 C>T, may be associated with individual susceptibility to hepatocellular carcinoma (HCC). However, the results remain conflicting rather than conclusive. Object. The aim of this study was to assess the association between miR-146a G>C and miR-196a2 C>T polymorphisms and the risk of HCC. Methods. A meta-analysis of 17 studies (10938 cases and 11967 controls) was performed. Odds ratios and 95% confidence intervals were used to evaluate the strength of the association. Results. For miR-146a G>C, the variant genotypes were associated with a decreased risk of HCC (CC versus GG: OR = 0.780 and 95% CI 0.700–0.869; GC/CC versus GG: OR = 0.865 and 95% CI 0.787–0.952; CC versus GC/GG: OR = 0.835 and 95% CI 0.774–0.901). For miR-196a2 C>T, significant association was also observed (TT versus CC: OR = 0.783, 95% CI: 0.649–0.943, and P = 0.010; CT versus CC: OR = 0.831, 95% CI 0.714–0.967, and P = 0.017; CT/TT versus CC: OR = 0.817, 95% CI 0.703–0.949, and P = 0.008). Conclusion. The two common polymorphisms miR-146a G>C and miR-196a2 C>T were associated with decreased HCC susceptibility, especially in Asian population.

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Section: Discussionsupporting

confidence: 87%

Association between Two Common Polymorphisms and Risk of Hepatocellular Carcinoma: Evidence from an Updated Meta-Analysis

Wang

Zhang

Shi

et al. 2014

BioMed Research International

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“…Several meta-analyses were conducted to investigate the association between miR-146a rs2910164 polymorphism and risks of various cancers (Wang et al, 2012;Wu et al, 2013;Xu et al, 2013;Yin et al, 2013), including liver cancer, gastric cancer, gallbladder cancer, breast cancer, and other cancers. However, the results were contradictory and inconclusive, and several studies about the relationship between rs2910164 polymorphisms and risks of digestive system cancers were published recently (Lv et al, 2013;Ma et al, 2013;Pavlakis et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

A Genetic Variant in MiR-146a Modifies Digestive System Cancer Risk: a Meta-analysis

Zhang²,

Mao³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…First, single nucleotide polymorphisms in selected miRNAs have been linked with heritable susceptibilities to disease; e.g. mutations in miR-146a and miR196a-2 increase susceptibility to human hepatocellular carcinoma (Xu et al, 2013). Second, epigenetic alterations to miRNA genes (including aberrant DNA methylation and histone modifications) alter miRNA expression in cancer and other diseases leading to the dysregulation of the expression of the mRNA targets of miRNAs (Suzuki et al, 2013).…”

Section: Reviewmentioning

confidence: 99%

Regulation of hypometabolism: insights into epigenetic controls

Storey

2015

Journal of Experimental Biology

144

129

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For many animals, survival of severe environmental stress (e.g. to extremes of heat or cold, drought, oxygen limitation, food deprivation) is aided by entry into a hypometabolic state. Strong depression of metabolic rate, often to only 1-20% of normal resting rate, is a core survival strategy of multiple forms of hypometabolism across the animal kingdom, including hibernation, anaerobiosis, aestivation and freeze tolerance. Global biochemical controls are needed to suppress and reprioritize energy use; one such well-studied control is reversible protein phosphorylation. Recently, we turned our attention to the idea that mechanisms previously associated mainly with epigenetic regulation can also contribute to reversible suppression of gene expression in hypometabolic states. Indeed, situations as diverse as mammalian hibernation and turtle anoxia tolerance show coordinated changes in histone post-translational modifications (acetylation, phosphorylation) and activities of histone deacetylases, consistent with their use as mechanisms for suppressing gene expression during hypometabolism. Other potential mechanisms of gene silencing in hypometabolic states include altered expression of miRNAs that can provide post-transcriptional suppression of mRNA translation and the formation of ribonuclear protein bodies in the nucleus and cytoplasm to allow storage of mRNA transcripts until animals rouse themselves again. Furthermore, mechanisms first identified in epigenetic regulation (e.g. protein acetylation) are now proving to apply to many central metabolic enzymes (e.g. lactate dehydrogenase), suggesting a new layer of regulatory control that can contribute to coordinating the depression of metabolic rate.

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Three common functional polymorphisms in microRNA encoding genes in the susceptibility to hepatocellular carcinoma: A systematic review and meta-analysis

Cited by 52 publications

References 37 publications

Association between Two Common Polymorphisms and Risk of Hepatocellular Carcinoma: Evidence from an Updated Meta-Analysis

Association between Two Common Polymorphisms and Risk of Hepatocellular Carcinoma: Evidence from an Updated Meta-Analysis

A Genetic Variant in MiR-146a Modifies Digestive System Cancer Risk: a Meta-analysis

Regulation of hypometabolism: insights into epigenetic controls

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