Background and purpose: DNA methylation is an important mechanism for regulating gene expression, and plays an important role in the tumorigenesis. Study shows that DNA methylation is a potentially promising biomarker in tumor diagnosis, prognosis as well as treatment selection. This study aimed to analyze the methylation status and assessed possible clinical value of 3 DNA repair genes BRCA1, GSTP1 and MGMT in breast cancer samples of Chinese women. Methods:Using methylation speciifc PCR (MSP), we analyzed the methylation status of 3 DNA repair genes BRCA1, GSTP1 and MGMT in 106 paired breast tumors and corresponding normal tissues. Results: The methylation rates of BRCA1, GSTP1 and MGMT were 24.5% (26/106), 29.2% (31/106) and 18.9%(20/106) in breast cancer tissues, which were higher than those (7.5%, 11.3%and 4.7%) in paired normal breast tissues, respectively (P<0.01). Methylation in at least one of the genes was found in 50.9%(54/106) of the breast cancer and 19.8%(21/106) in paired normal breast tissues. And the mean number of genes hypermethylated in each tumor and paired normal breast tissues were 0.73 and 0.24, respectively (P<0.000 1). The methylation status of BRCA1 was more frequent in the younger patients than in the older patients (P=0.007) and most BRCA1 methylated patients were ER negative (P=0.020). Methylation status of GSTP1 was signiifcantly correlated with tumor size, lymph node metastasis (P=0.028 and 0.033, respectively). MGMT methylation was significantly correlated with tumor stage, higher tumor grade and lymph node metastasis (P=0.016, 0.025 and 0.030, respectively). High frequency simultaneous methylation of these 3 genes was more often in those with higher tumor stage and lymph node metastasis (P=0.028 and 0.007, respectively). Conclusion:Hypermethylation of BRCA1, GSTP1 and MGMT genes may be linked to various known clinicopathological features of breast cancer in Chinese women, and the increasing multiple gene methylation in tumors may indicate an aggressive phenotype for breast cancer. Detection of the methylation status of these genes may be useful for identifying patients at high risk for breast cancer.

Study found that in some human tumors such as breast cancer,SOX7 gene is highly likely to be a tumor suppressor gene.The tumor suppressor role of SOX7 may be accomplished by regulating the Wnt/β-catenin signaling pathway mediated the transcription process,and the abnormal Wnt/β-catenin signaling pathway is likely to play its role through the regulation of its downstream target gene Cyclin D1,etc,so that the ahnormal cell proliferation activity is unable to carry on,and thus plays the function of tumor suppressor.This review will summarize the research progress of the role of SOX7 geue and its closely related β-catenin,Cyclin D1 gene in breast cancer.

Background and purpose:Aberrant DNA methylation that leads to the inactivation of tumor suppressor genes plays important roles in development and progression of breast cancer. Clinically, related gene methylation is considered to be a promising biomarker for tumor diagnosis and prognosis. This study aimed to investigate the methylation status ofSox17 gene in breast cancer tissue and its corresponding plasma circulating DNA, as well as to investigate its value in breast cancer early diagnosis and prognosis.Methods:TheSox17 gene promoter methylation status was detected by MSP in 86 cases of breast cancer, 36 normal breast tissues and its paired plasma DNA, the results were analyzed with corresponding clinical and pathological features.Results:The frequency ofSox17 gene methylation rate among 86 breast cancer tissues was 77.9%(67/86), and was 61.6%(53/86)in plasma circulating DNA, however, noSox17 gene methylation was found in normal breast tissues.Sox17 gene promoter methylation in plasma circulating DNA was signiifcantly associated with the methylation status in tumor tissues (r=0.502,P=0.000). In breast cancer tissue specimens,Sox17 methylation status was significantly correlated with tumor stage (χ2=6.18,P=0.041) and lymph node metastasis (χ2=13.54,P=0.001);Sox17 gene methylation rate was signiifcantly correlated with tumor stage (χ2=27.06,P=0.000), tumor size (χ2=9.65,P=0.007) and lymph node metastasis (χ2=20.80,P=0.000) in plasma samples, and there was no signiifcant difference ofSox17 gene methylation between patient age, histological grade and ER, PR, HER-2/neu status.Conclusion:Sox17 gene promoter methylation plays an important role in the carcinogenesis and development of breast cancer, and may be associated with the prognosis of breast cancer. Furthermore, methylatedSox17 gene may be a useful tumor biomarker in plasma circulating DNA for breast cancer detection and disease monitoring.

Breast cancer is one of the most common malignant tumors in clinic,and its pathogenesis has been extensively studied by people.miRNA play an important regulatory role in normal breast cell proliferation and apoptosis,they are widely involved in the occurrence and development of breast cancer and are attracting more and more attention as new tumor markers.The Wnt/β-catenin signaling pathways involved in breast cancer and other malignancies have long been confirmed.Recent studies have shown that a variety of important members of the Wnt/β-catenin signaling pathway can be regulated as miRNA target genes,affecting the occurrence and development of breast cancer.At the same time,Wnt/β-catenin signaling pathway changes can also cause the expression of related miRNA changes.Both miRNA and Wnt/ β-catenin signaling pathways play an important regulatory role in the pathogenesis of breast cancer,but the complex regulatory relationship between them has not been elucidated yet.Therefore,in this review,the roles of miRNA and Wnt/β-catenin signaling in breast cancer and its relationship with each other are reviewed in order to gain a deeper understanding of the complex pathogenesis of breast cancer and to explore new diagnostic molecular markers and therapeutic targets for breast cancer,provide a new idea for the diagnosis and treatment of breast cancer.

In order to study effects of ginseng on the metabolism of drug belong to CYP3A4 substrate, screening of pregnane X receptor activation from ginsenosides was performed by reporter assay. Based on PXR-CYP3A stable translation cell lines, 13 ginsenosides were screened for pregnane X receptor activation by reporter assays, and RIF as the positive control. The effect of ginsenosides Rg1 onCYP3A4 mRNA expression was also investigated by RT-PCR. The PXR-CYP3A stable translation cell lines had good response to RIF, and the EC50 is 2.51 micro mol x L(-1). When the condition of final concentration was 10 micromol x L(-1), ginsenoside F2 and protopanaxatriol had moderate inductive effects on PXR. Panaxotriol, Rg2, pseudoginsenoside F11, Rg1, ginsenoside and Rb3 had inhibitory effects on PXR. Ginsenoside Rf1, Rg3, Rh2 and protopanaxdiol had no obvious effects on PXR. Rg1 down-regulated CYP3A4 mRNA expression in a concentration-dependent manner. Activation of pregnane X receptor by ginsenosides may influence the metabolism of drug belong to CYP3A4 substrate, and cause ginseng-drug interactions.

Epithelial mesenchymal transition is a kind of important pathophysiological phenomenon,which refers to a biological processe that epithelial cell turns into another cell with mesenchymal phenotype undergoing a specific procedure.Once the tumor cell acquires mesenchymal cell molecular phenotype,it will enable stationary epithelial cells to gain the ability to migrate and invade as single cells,being easy to break away from the original tumor and move to the distal organs with blood flow.The occurrence of epithelial mesenchymal transition involves a variety of signal transduction pathways,which relates to inducing factors,transcription factors and so on.The occurrence and development of breast cancer is influenced by many factors and many signal transduction pathways.In recent years,the research of tumor suppressor and tumor resistance is more extensive.In this paper,a review of epithelial mesenchymal transition related signaling pathways in breast cancer is presented.