Wang Z.,Nanjing Medical University |
Cui D.,Henan Tumor Institute |
Cui D.,Zhengzhou University |
Lu W.,Henan Tumor Institute
Breast Cancer Research and Treatment | Year: 2010
NBS1 gene plays an important role in DNA repair. Many epidemiological studies have investigated the association between NBS1 8360G > C polymorphism and breast cancer, however, the results are still controversial. Therefore, we performed a meta-analysis of 10 case-control studies. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of the association. The results showed NBS1 8360G > C polymorphism contributed to breast risk in overall populations (for CC vs. GG: OR = 0.75, 95% CI = 0.74-0.98, P = 0.13 for heterogeneity; for the recessive model CC vs. GG/CG: OR = 0.88, 95% CI = 0.77-1.00, P = 0.44 for heterogeneity). In subgroup analysis by ethnicity, no significant association was found in all genetic models. In summary, our meta-analysis strongly suggests the NBS1 8360G > C polymorphism is associated with breast cancer. © 2010 Springer Science+Business Media, LLC.
Wang T.,Henan University of Traditional Chinese Medicine |
Xuan X.,Zhengzhou University |
Pian L.,Henan University of Traditional Chinese Medicine |
Gao P.,Henan University of Traditional Chinese Medicine |
And 4 more authors.
Tumor Biology | Year: 2014
Notch has recently been shown to promote epithelial-to-mesenchymal transition (EMT) by involving in the EMT process that occurs during tumor progression and converts polarized epithelial cells into motile, invasive cells. However, it is still unclear whether the Notch signaling pathway is associated with the regulation of EMT in esophageal carcinoma. The present study explored Notch-1-mediated esophageal carcinoma EC-9706 cell invasion and metastasis by inducing epithelial-mesenchymal transition through Snail. The results demonstrated that the inhibition of Notch-1 expression in the esophageal carcinoma cell line EC-9706 could suppress the occurrence of EMT and at the same time could decrease the invasion and metastasis ability of the EC-9706 cells, indicative of its role in EMT. Snail is a transcriptional repressor of E-cadherin. We found that with the inhibition of Notch-1 expression in the esophageal carcinoma cell line EC-9706, the expression of Snail also decreased. Mechanistic studies showed that the up-expression of Snail in the EC-9706 cells restored the suppression of EMT regulated by Notch-1 inhibition, suggesting the role of Snail in Notch-1-mediated EMT. At the same time, the up-expression of Snail in the EC-9706 cells could also rescue the invasion and metastasis ability inhibited by Notch-1 siRNA. Taken together, our results had revealed that Notch-1 could participate in the invasion and metastasis of esophageal carcinoma through EMT via Snail. This study indicated that Notch-1 might be a useful target for esophageal carcinoma prevention and therapy. © International Society of Oncology and BioMarkers (ISOBM) 2013.
Wang T.,Zhengzhou University |
Mi Y.,Zhengzhou University |
Pian L.,The First Affiliated Hospital College |
Gao P.,Zhengzhou University |
And 3 more authors.
Diagnostic Pathology | Year: 2013
CXC chemokine receptor 4 was found to be expressed by many different types of human cancers and its expression has been correlated with tumor aggressiveness, poor prognosis and resistance to chemotherapy. However the effect of CXCR4 on the esophageal carcinoma cells remains unclear, the present study explored the effects of CXCR4 siRNA on proliferation and invasion of esophageal carcinoma KYSE-150 and TE-13 cells. Two siRNA sequence targeting CXCR4 gene were constructed and then were transfected into KYSE-150 and TE-13 cells by Lipofectamine™2000. Changes of CXCR4 mRNA and protein were analyzed by qRT-PCR and Western blot. Effect of CXCR4 siRNA on KYSE-150 and TE-13 cells proliferation was determined by MTT. Transwell invasion assay was used to evaluate the invasion and metastasis of KYSE-150 and TE-13 cells. Tumor growth was assessed by subcutaneous inoculation of cells into BALB/c nude mice. qRT-PCR and Western blot demonstrate that the expression level of CXCR4 gene were obviously decreased in KYSE-150 and TE-13 cells transfected with CXCR4 targeting siRNA expression vectors. The average amount of cells transfected with CXCR4 siRNA penetrating Matrigel was significantly decreased (p<0.05). Injection of CXCR4 siRNA transfected cells inhibited tumor growth in a xenograft model compared with blank and negative control groups (p <0.05). CXCR4 silenced by siRNA could suppress the proliferation, invasion and metastasis of esophageal carcinoma cell lines KYSE-150 and TE-13 in vitro and in vivo. The results provide a theoretical and experimental basis for the gene therapy of ESCC using RNAi technology based on CXCR4 target site. Virtual slides: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/3502376691001138. © 2013 Wang et al.; licensee BioMed Central Ltd.
Zhao E.,Zhengzhou University |
Cui D.,Zhengzhou University |
Yuan L.,Henan Tumor Hospital |
Lu W.,Henan Tumor Institute
Molecular Biology Reports | Year: 2012
The mouse double minute 2 (MDM2) gene encodes a phosphoprotein that interacts with P53 and negatively regulates its activity. SNP309 polymorphism (T-G) in the promoter of MDM2 gene has been reported to be associated with enhanced MDM2 expression and tumor development. Many published studies have evaluated the association between MDM2 SNP309 polymorphism and breast cancer risk. However, the results were inconsistent. We combined and analyzed the data from 19 case-control studies including 14,450 cases and 13,382 controls. Crude odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of the association between MDM2 SNP309 polymorphism and breast cancer risk. No significant association was found in all genetic models in overall population. However, in subgroup analysis by ethnicity (4 studies in Asian group, 13 studies in European group, 2 studies of mixed population which were separated into 2 European population group and 2 African population group), we found an increased breast cancer susceptibility for GT versus TT (OR = 1.31, 95% CI = 1.03-1.67) in Asian population and for GT versus TT (OR = 1.31, 95% CI = 1.03-1.66) in African population. When stratified by family history status (5 studies in familial breast cancer group, 5 studies in sporadic breast cancer group), homozygous subjects of sporadic breast cases carrying the T309G G allele exhibited elevated breast cancer risk (OR = 1.35, 95% CI = 1.00-1.82), whereas heterozygous carriers did not show significant association with breast cancer risk for GT vs. TT (OR = 1.26, 95% CI = 0.84-1.87). Our meta-analysis suggests that MDM2 SNP309 polymorphism may increase the risk to breast cancer in Asian and African population. © Springer Science+Business Media B.V. 2011.
Yang Q.,Henan University |
Li M.,Zhengzhou University |
Wang T.,Henan University |
Xu H.,Henan Tumor Institute |
And 2 more authors.
Diagnostic Pathology | Year: 2013
Background: STAT is the backward position of cytokine and growth factor receptors in the nucleus, STAT dimers could bind to DNA and induce transcription of specific target genes. Several lines of evidence support the important roles of STAT, especially STAT5, in carcinogenesis. The overexpression of STAT 5 is related to the differentiation and apoptosis of tumor cells. However, the role of STAT5 in esophageal squamous cell carcinoma remains unclear.Methods: The siRNA vectors aiming to STAT5 gene were constructed. STAT5 siRNA was transfected into Eca-109 cells by Lipofectamine™2000. Expression of STAT5, Bcl-2 and Cyclin D1 were analyzed by Western blot and RT-PCR. Eca-109 cells proliferation was determined by MTT. Eca-109 cell cycle and apoptosis were detected by the flow cytometry. Boyden chamber was used to evaluate the invasion and metastasis capabilities of Eca-109 cells.Results: The double strands oligonucleotide of siRNA aiming to STAT5 was successfully cloned into the pRNAT-U6.1 vector, and the target sequence coincided with the design. RT-PCR and Western blotting detection demonstrated that the expression levels of STAT5, Bcl-2 and Cyclin D1 gene were obviously decreased in Eca-109 cells transfected with STAT5 siRNA. STAT5 siRNA could suppress the proliferation of Eca-109 cells. The proportion of S and G2/M period frequency was significantly decreased (p < 0.05). The proportion of G0/G1 period frequency was significantly increased (p < 0.05). The average amount of cells penetrating Matrigel was significantly decreased (p < 0.05).Conclusions: STAT5 silenced by siRNA could induce the apoptosis and suppress the proliferation, invasion and metastasis of esophageal carcinoma cell line Eca-109, which indicated STAT5 might be a novel therapeutic strategy for the human ESCC.Virtual slides: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1351913072103000. © 2013 Yang et al.; licensee BioMed Central Ltd.