Protein kinase D1 inhibits breast cancer cell invasion via regulating matrix metalloproteinase expression.

PURPOSE: This study aimed to explore the role of protein kinase D1 (PKD1) in breast cancer invasion. MATERIALS AND METHODS: The relative expression of PKD1mRNA and protein in human invasive breast cancer tissue samples and normal samples, as well as breast cancer cell lines, were detected. Constitutively-active PKD1 and PKD1 specific shRNA were expressed in the MD-MB-231 and MCF-7 cells, respectively. The role of PKD1 in the invasive behavior of breast cancer cell line was evaluated by matrix metalloproteinase (MMP) expression. RESULTS: The results showed that PKD1, as a serine/threonine kinase, is downregulated significantly in invasive ductal carcinoma and metastatic invasive ductal carcinoma tissue than the normal tissue and the low expression of PKD1 is also found in breast cancer cell line MD-MB-231. The MMP2 and MMP9 expression in PKD1 constitutively-active MD-MB-231 cells and MCF-7 knockdown cells were decreased and increased respectively. CONCLUSION: The authors confirmed that PKD1 was downregulated in invasive breast cancer. PKD1 can negatively regulate the MMP expression and may serve as a potential therapeutic target.

Screening for key genes associated with invasive ductal carcinoma of the breast via microarray data analysis.

The aim of this study was to identify key genes related to invasive ductal carcinoma (IDC) of the breast by analyzing gene expression data with bioinformatic tools. Microarray data set GSE31138 was downloaded from Gene Expression Omnibus, including 3 breast cancer tissue samples and 3 normal controls. Differentially expressed genes (DEGs) between breast cancer and normal control were screened out (FDR < 0.05 and |logFC| > 2). Coexpression between genes was examined with String, and a network was then constructed. Relevant pathways and diseases were retrieved with KOBAS. A total of 56 DEGs were obtained in the IDC of the breast compared with normal controls. A gene coexpression network including 27 pairs of genes was constructed and all the genes in the network were upregulated. Further study indicated that most of the genes in the coexpression network were enriched in ECM-receptor interaction (COL4A2, FN1, and HMMR) and nucleotide excision repair (CETN2 and PCNA) pathways, and that the most significantly related disease was autoimmune lymphoproliferative syndromes. A number of DEGs were acquired through comparative analysis of gene expression data. These findings are beneficial in promoting the understanding of the molecular mechanisms in breast cancer. More importantly, some key genes were revealed via gene coexpression network analysis, which could be potential biomarkers for IDC of the breast.

[Study on auto-solidified tumor vaccine].

In order to evaluate the immune effect of Auto-solidified tumor vaccine induced by thermal doses of 65 degrees C for 5 minutes on the killing and inactivation of cancer cells in operation, a series of experimental and clinical studies were carried out, the results showed that Balb/c mice immunized with ASTV could tolerate the aggression of H22 3 x 10(8) cancer cells with efficiency of 93.3% (28/30), the inoperable advanced hepatic cancer proved in operation was hypothermited and ASTV was made for immune injection postoperatively, with the clinical efficiency 76.8% (53/69), and 5-year survival rate 23% (9/39), the difference with control group is significant. In recent years, it is recognized once again that tumor can induce specific immunity. The most important matter is how to stimulate the host to produce effective cellular immunity. Our results showed that the thermal biological effect could inactivate cancer cell and change nuclear antigen in host net-like immunity system. Under gene regulation, the host can obtain the cellular immune effect against cancer cells.