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Ma C.,Changning Maternity and Infant Health Hospital of Shanghai | Liu Y.,Changning Maternity and Infant Health Hospital of Shanghai | Zhang W.,Changning Maternity and Infant Health Hospital of Shanghai | Liu P.,Changning Maternity and Infant Health Hospital of Shanghai
Molecular Biology Reports | Year: 2013

Methylenetetrahydrofolate reductase (MTHFR) enzyme plays an important role in folate metabolism and MTHFR polymorphisms have been suggested to be associated with risk of various cancers. MTHFR C677T polymorphism is a common genetic alteration and may affect the host susceptibility to ovarian cancer. The aim of this study was to investigate the association between MTHFR C677T polymorphism and ovarian cancer risk by performing a meta-analysis. Pubmed, Embase, Web of Science and Chinese Biomedical Database (CBM) databases were searched for case-control studies investigating the association between MTHFR C677T polymorphism and ovarian cancer. Odds ratio (OR) and its 95 % confidence interval (95 % CI) was used to assess this possible association. 13 individual case-control studies from 10 publications with a total of 18, 628 subjects (5, 932 cases and 12, 696 controls) were included into this meta-analysis. Meta-analyses showed there was no association between MTHFR C677T polymorphism and ovarian cancer risk in Caucasians under all five genetic models (All P values for the pooled ORs were more than 0.05), whereas there was an obvious association between MTHFR C677T polymorphism and ovarian cancer risk in Asians under four genetic models (for T vs C, OR (95 % CI) = 1.38(1.19-1.61); for TT vs CC, OR (95 % CI) = 2.32(1.63-3.29); for TT vs TC+CC, OR (95 % CI) = 2.04(1.47-2.85); for TT+TC vs CC, OR (95 % CI) = 1.36(1.12-1.65)). Subgroup analyses suggested ethnicity was the major source of heterogeneity. This meta-analysis supports an association between MTHFR C677T polymorphism and ovarian cancer risk, and there might be a race-specific effect in this association. Further studies with large sample size and careful design are needed to identify this association more comprehensively. © 2013 Springer Science+Business Media Dordrecht. Source


Lao G.,Changning Maternity and Infant Health Hospital of Shanghai | Liu P.,Changning Maternity and Infant Health Hospital of Shanghai | Wu Q.,Changning Maternity and Infant Health Hospital of Shanghai | Zhang W.,Changning Maternity and Infant Health Hospital of Shanghai | And 3 more authors.
Tumor Biology | Year: 2014

MicroRNAs (miRNAs) are important regulators of many physiological and pathological processes, including cell proliferation, apoptosis, and cell cycle arrest. In this study, we aimed to investigate the biological role of miR-155 in cervical cancer and the underlying molecular mechanism involved in tumorigenesis. The expression of miR-155 in human cervical cancer tissues was detected by real-time PCR. MTT assay and BrdU incorporation assay were used to measure the proliferation of cervical cancer cells. Apoptosis cells and cell cycle distribution were analyzed by flow cytometry. We found that the expression of miR-155 was upregulated in cervical cancer tissues compared to the adjacent non-cancer tissues. Overexpression of miR-155 promoted the proliferation of Hela and SiHa cells. By contrast, downregulation of miR-155 inhibited the growth of cervical cancer cells. Flow cytometry analysis showed that low expression of miR-155 promoted apoptosis and induced cell cycle arrest in Hela and SiHa cells. Moreover, the mRNA and protein expression of LKB1 was significantly reduced in cervical cancer tissues. Luciferase reporter assay demonstrated that LKB1 was a target gene of miR-155, suggesting that miRNA-155 promoted the proliferation of cervical cancer cells by regulating LKB1 expression. © 2014 International Society of Oncology and BioMarkers (ISOBM). Source

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