p27<sup>Kip1</sup> V109G Polymorphism and Cancer Risk: A Systematic Review and Meta-Analysis

Feng, Wei; Xu, Jin; Tang, Lin; Shao, Jia-Qing; Wang, Yucai; Chen, Longbang; Guan, Xiaoxiang

doi:10.1089/cbr.2012.1229

Cited by 22 publications

(22 citation statements)

References 28 publications

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“…When no statistical heterogeneity was found (I 2 <40% or P (Q)>0.10), the ORs and 95%CI would be estimated for each study in the fixed-effect model. Otherwise, the random-effect model was applied (Ding et al, 2011;Pan et al, 2013;Wei et al, 2013;. Statistical tests were performed using the program Review Manager5.0 software.…”

Section: Discussionmentioning

confidence: 99%

PLCE1 rs2274223 Polymorphism and Susceptibility to Esophageal Cancer: a Meta-analysis

Guo

Yang²,

Hu³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Purpose: To investigate and study the relationship between the PLCE1 rs2274223 gene polymorphism and susceptibility to esophageal cancer by meta-analysis. Materials and Methods: The literature was searched in Wanfang, CNKI, PubMed, CBM, Web of Science, MEDLINE, EMBASE, Springer, Elsevier and Cochrane databases from the date of January 1 st 2004 to April 1 st 2014 to collect case-control studies on the PLCE1 polymorphism and susceptibility to esophageal cancer. For the population genotype distributions of both esophagus cancer and control groups, their odds ratios (ORs) and 95% confidence intervals (CIs) were taken as effect indexes. Disqualified studies were excluded. Odds ratios of PLCE1 rs2274223 genotype distributions in the group of patients with esophageal cancer and the group of healthy control were calculated. The metaanalysis software, RevMan5.0, was applied for heterogeneity test, pooled OR and 95% confidence intervals. Sensitivity analysis and publication bias were also explored. Results: A total of twelve case-control studies were included, covering a total of 9, 912 esophageal cancer cases and 13, 023 controls were included. The pooled odds ratio of PLCE1 rs2274223 genotype GA vs AA was 1.29 (95%CI=1.17~1.43), p<0.01, GG vs AA was 1.65 (95%CI=1.32~2.05), p<0.01, GG/GA vs AA was 1.30 (95%CI=1.16~1.46), p<0.01 and GG vs GA/AA was 1.48 (95%CI=1.22~1.80), p<0.01. The PLCE1 rs2274223 polymorphism was thus associated with risk of esophageal cancer in all genetic models. In the stratified analysis by ethnicity, and source of controls, no significantly increased risk was observed for white persons. There was no obvious publication bias detected. Conclusions: This meta-analysis showed there was a significantly association between PLCE1 rs2274223 polymorphism and esophageal cancer in yellow race populations. Due to some minor limitations, our findings should be confirmed in further studies.

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Section: Discussionmentioning

confidence: 99%

PLCE1 rs2274223 Polymorphism and Susceptibility to Esophageal Cancer: a Meta-analysis

Guo

Yang²,

Hu³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…The occurrence, development, and metastasis of BC are closely associated with mutations in a variety of genes, alterations in cell signaling pathways, and neovascular dysplasia (Qin et al, 2012;Wei et al, 2012). MiRNAs act as "hackers" in the field of genetic research, as they regulate up to 30% of the protein-coding genes in humans.…”

Section: Discussionmentioning

confidence: 99%

MiRNA-15a Mediates Cell Cycle Arrest and Potentiates Apoptosis in Breast Cancer Cells by Targeting Synuclein-γ

Xie²,

Chen³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Background: Recent studies have indicated that microRNA-15a (miR-15a) is dysregulated in breast cancer (BC). We aimed to evaluate the expression of miR-15a in BC tissues and corresponding para-carcinoma tissues. We also focused on effects of miR-15a on cellular behavior of MDA-MB-231 and expression of its target gene synuclein-γ (SNCG). Materials and Methods: The expression levels of miR-15a were analysed in BC formalin fixed paraffin embedded (FFPE) tissues by microarray and quantitative real-time PCR. CCK-8 assays, cell cycle and apoptosis assays were used to explore the potential functions of miR-15a in MDA-MB-231 human BC cells. A luciferase reporter assay confirmed direct targets. Results: Downregulation of miR-15a was detected in most primary BCs. Ectopic expression of miR-15a promoted proliferation and suppressed apoptosis in vivo. Further studies indicated that miR-15a may directly interact with the 3'-untranslated region (3'-UTR) of SNCG mRNA, downregulating its mRNA and protein expression levels. SNCG expression was negatively correlated with miR-15a expression. Conclusions: MiR-15a has a critical role in mediating cell cycle arrest and promoting cell apoptosis of BC, probably by directly targeting SNCG. Thus, it may be involved in development and progression of BC.

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“…A recent meta-analysis has evaluated the association data of eight studies encompassing 3799 controls and 3591 patients with non-endocrine tumors (oral squamous cell, prostate, breast cancer, and pancreatic cancer) and found no correlation between the rs2066827 variant and the overall cancer risk in the general population (Wei et al 2012). Since p27 is a tumor susceptibility gene for multiple endocrine tumors in both humans and rats, we decided to investigate specifically endocrine tumors.…”

Section: Discussionmentioning

confidence: 99%

p27 variant and corticotropinoma susceptibility: a genetic and in vitro study

Sekiya

Bronstein

Benfini

et al. 2014

Endocrine-Related Cancer

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Germline mutations in p27 kip1 are associated with increased susceptibility to multiple endocrine neoplasias (MEN) both in rats and humans; however, the potential role of common polymorphisms of this gene in endocrine tumor susceptibility and tumorigenesis remains mostly unrecognized. To assess the risk associated with polymorphism rs2066827 (p27-V109G), we genotyped a large cohort of Brazilian patients with sporadic endocrine tumors (pituitary adenomas, nZ252; pheochromocytomas, nZ125; medullary thyroid carcinoma, nZ51; and parathyroid adenomas, nZ19) and 885 population-matched healthy controls and determined the odds ratios and 95% CIs. Significant associations were found for the group of patients with pituitary adenomas (PZ0.01), particularly for those with ACTH-secreting pituitary adenomas (PZ0.005). In contrast, no association was found with GH-secreting pituitary tumors alone or with the sporadic counterpart of MEN2-component neoplasias. Our in vitro analyses revealed increased colony formation and cell growth rate for an AtT20 corticotropin mouse cell line overexpressing the p27-V109G variant compared with cells transfected with the WT p27. However, the genotypic effects in genetic and in vitro approaches were divergent. In accordance with our genetic data showing specificity for ACTH-secreting pituitary tissues, the overexpression of p27-V109G in a GH3 somatotropin rat cell line resulted in no difference compared with the WT. Pituitary tumors are one of the major clinical components of syndromes associated with the p27 pathogenic mutations MENX and MEN4. Our genetic and in vitro data indicate that the common polymorphism rs2066827 may play a role in corticotropinoma susceptibility and tumorigenesis through a molecular mechanism not fully understood thus far.

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p27^Kip1 V109G Polymorphism and Cancer Risk: A Systematic Review and Meta-Analysis

Cited by 22 publications

References 28 publications

PLCE1 rs2274223 Polymorphism and Susceptibility to Esophageal Cancer: a Meta-analysis

PLCE1 rs2274223 Polymorphism and Susceptibility to Esophageal Cancer: a Meta-analysis

MiRNA-15a Mediates Cell Cycle Arrest and Potentiates Apoptosis in Breast Cancer Cells by Targeting Synuclein-γ

p27 variant and corticotropinoma susceptibility: a genetic and in vitro study

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p27Kip1 V109G Polymorphism and Cancer Risk: A Systematic Review and Meta-Analysis

Cited by 22 publications

References 28 publications

PLCE1 rs2274223 Polymorphism and Susceptibility to Esophageal Cancer: a Meta-analysis

PLCE1 rs2274223 Polymorphism and Susceptibility to Esophageal Cancer: a Meta-analysis

MiRNA-15a Mediates Cell Cycle Arrest and Potentiates Apoptosis in Breast Cancer Cells by Targeting Synuclein-γ

p27 variant and corticotropinoma susceptibility: a genetic and in vitro study

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p27^Kip1 V109G Polymorphism and Cancer Risk: A Systematic Review and Meta-Analysis