The E-cadherin (CDH1) −160 C/A polymorphism and prostate cancer risk: a meta-analysis

Qiu, Lixin; Li, Rutian; Zhang, Jianbing; Zhong, Wen‐Zhao; Bai, Jianling; Liu, Baorui; Zheng, Ming‐Hua; Qian, Xiaoping

doi:10.1038/ejhg.2008.157

Cited by 35 publications

(21 citation statements)

References 29 publications

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“…A stratified analysis by cancer type indicated that rs16260 AA genotype increased risk of prostate cancer, which was consistent with results for the previous study (Qiu et al, 2008), but no significant associations were observed in breast cancer and gastric cancer, which revealed that rs16260 polymorphism might have different effects on distinct cancers. Otherwise, results appeared in gastric cancer were inconsistent with previous studies (Cui et al, 2011;Corso et al, 2012;Li et al, 2012), which might be caused by limited studies enrolled in the present meta-analysis.…”

Section: Discussionsupporting

confidence: 80%

“…Finally, the results, for a stratified analysis by source of controls, indicated that different sources of controls played different roles in cancer risk by the stratified analysis. A significant association with increased cancer risk was discovered for population-based controls, which was inconsistent with the previous study (Qiu et al, 2008;. As population-based controls usually represented the healthy population, but there were the sick people in the hospital-based controls, a proper and representative population-based controls should enrolled in the further studies to make the results more dependable.…”

Section: Discussioncontrasting

confidence: 52%

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Roles of E-Cadherin (CDH1) Genetic Variations in Cancer Risk: a Meta-analysis

Deng¹,

He²,

Pan³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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E-Cadherin (CDH1) genetic variations may be involved in invasion and metastasis of various cancers by altering gene transcriptional activity of epithelial cells. However, published studies on the association of CDH1 gene polymorphisms and cancer risk remain contradictory, owing to differences in living habits and genetic backgrounds. To derive a more better and comprehensive conclusion, the present meta-analysis was performed including 57 eligible studies of the association between polymorphisms of CDH1 gene promoter -160 C>A, -347 G>GA and 3'-UTR +54 C>T and cancer risk. Results showed that these three polymorphisms of CDH1 were significantly associated with cancer risk. For -160 C>A polymorphism, -160A allele carriers (CA and CA+AA) had an increased risk of cancer compared with the homozygotes (CC), and the similar result was discovered for the -160A allele in the overall analyses. In the subgroup analyses, obvious elevated risk was found with -160A allele carriers (AA, CA, CA+AA and A allele) for prostate cancer, while a decreased colorectal cancer risk was shown with the AA genotype. For the -347 G>GA polymorphism, the GAGA genotype was associated with increased cancer risk in the overall analysis with homozygous and recessive models. In addition, results of subgroup analysis indicated that the elevated risks were observed in colorectal cancer and Asian descendants. For +54 C>T polymorphism, a decreased risk of cancer was found in heterozygous, dominant and allele models. Moreover, +54T allele carriers (CT, CT+TT genotype and T allele) showed a potential protective factor in gastric cancer and Asian descendants.

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Section: Discussionsupporting

confidence: 80%

Section: Discussioncontrasting

confidence: 52%

Roles of E-Cadherin (CDH1) Genetic Variations in Cancer Risk: a Meta-analysis

Deng¹,

He²,

Pan³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…In this complex, β-catenin and p120 are directly associated with E-cadherin, while α-catenin is the link between β-catenin and actin microfilament network of the cytoskeleton (21, 22). Importantly, the aberrant or decreased expression of E-cadherin is considered as one of the biomarkers for poor prognosis in PCA (23, 24). Therefore, promoting E-cadherin expression using non-toxic phytochemicals should be considered an ideal strategy towards preventing cancer cells from acquiring motility and invasiveness.…”

Section: Introductionmentioning

confidence: 99%

Role of E-cadherin in Antimigratory and Antiinvasive Efficacy of Silibinin in Prostate Cancer Cells

Deep

Gangar

Agarwal

et al. 2011

Cancer Prevention Research

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The epithelial-to-mesenchymal transition (EMT) in prostate cancer (PCA) cells is considered pre-requisite for acquiring migratory/invasive phenotype, and subsequent metastasis. We hypothesized that promoting the E-cadherin expression in PCA cells by using non-toxic phytochemicals, like silibinin, would prevent EMT and consequently invasiveness. Our results showed that silibinin treatment (5–90 µM) significantly inhibits migratory and invasive potential of advance human PCA PC3, PC3MM2 and C4-2B cells in in vitro assays. Importantly, the anti-migratory/anti-invasive efficacy of silibinin was not due to its cytotoxicity towards PCA cells. Molecular analyses showed that silibinin increases E-cadherin level that was localized mainly at cellular membrane as evidenced by sub-cellular fractional and confocal analyses in PC3 cells, which might be responsible for morphologically observed shift towards epithelial character. Silibinin also decreased the levels of Slug, Snail, phospho-Akt(ser473), nuclear β-catenin, phospho-Src(tyr419) and Hakai; together they play important role in regulating E-cadherin expression/function and EMT. Similar silibinin effects on E-cadherin, β-catenin, phospho-Src(tyr419) and Hakai levels were also observed in PC3MM2 and C4-2B PCA cells. Selective Src inhibition by dasatinib also showed increased E-cadherin expression in PC3 cells suggesting a possible involvement of Src inhibition in silibinin-caused increase in E-cadherin level. Additional studies in PC3 cells with stable knock-down of E-cadherin expression revealed that anti-migratory/anti-invasive efficacy of silibinin is in-part dependent on E-cadherin expression. Together, our results showing anti-migratory/anti-invasive effects of silibinin and associated mechanisms suggest that silibinin should be tested further in clinically relevant animal models towards exploiting its potential benefits against metastatic PCA.

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“…It is thought that SNPs contribute to interindividual variability in susceptibility to common diseases such as cancer [35,36]. So far, some published meta-analyses have confirmed that a number of SNPs are associated with increased or decreased PCa risk in different races, such as A49T in steroid-5-alpha-reductase, alpha polypeptide 2 (SRD5A2) gene [37], Gly388Arg in fibroblast growth factor receptor 4 (FGFR4) gene [38], -160C/A in E-cadherin (CDH1) gene [39], Val16Ala in manganese superoxide dismutase (MnSOD) gene [40], C677T in 5,10-methylenetetrahydrofolate reductase (MTHFR) gene [41]. Several studies have investigated the possible role of anti-tumor gene polymorphisms and the prevalence of PCa.…”

Section: Discussionmentioning

confidence: 99%