Project description:Transcripts upregulated or downregulated by knockdown of MUC1 were identified through expression profiling of a total of 12,135 genes in comparison with MKN45- MUC1 RNAi clones and control clones. We endeavored to identify genes which expression is affected by MUC1 by performing cDNA microarray analysis on two MKN45 MUC1 RNAi clones and one control clone.
Project description:Transcripts upregulated or downregulated by knockdown of MUC1 were identified through expression profiling of a total of 12,135 genes in comparison with MKN45- MUC1 RNAi clones and control clones.
Project description:Expression of SET7/9, a histone methyltransferase, was frequently reduced in cultured and primary gastric cancers. To identify the SET7/9 target genes in gastric cancer, we performed siRNA-based knockdown of SET7/9 in MKN74 and MKN45 cells and then examined significant expression changes of genes by microarray. Transfection of SET7/9 siRNA into MKN74 and MKN45 cells were performed by electroporation. After 48hrs, cells were harvested. Total RNA was used for cDNA microarray.
Project description:Expression analysis of gene expression changes in Homo sapiens SGC-7901 cells after knock down of MTA2 (Metastasis-associated protein) or overexpression SNHG5 (snoRNA host gene 5) Investigation of whole genome gene expression level changes in a Homo sapiens gastric carcinoma cells SGC-7901 after knock down MTA2 expression and upregulation of SNHG5
Project description:Expression of SET7/9, a histone methyltransferase, was frequently reduced in cultured and primary gastric cancers. To identify the SET7/9 target genes in gastric cancer, we performed siRNA-based knockdown of SET7/9 in MKN74 and MKN45 cells and then examined significant expression changes of genes by microarray.
Project description:In contrast to the decreasing trends in developed countries, the incidence and mortality rates of cervical cancer in China have increased significantly. Screening and identification of reliable biomarkers and candidate drug targets of cervical cancer are urgent to improve the survival rate and quality of life of patients. In this study, we demonstrated that MUC1 displayed elevation in cervical squamous cell carcinoma (CSCC). The expression of MUC1 was higher in neoplastic compared with non-neoplastic tissues of the cervix, indicated its potential in early diagnosis of cervical squamous cell carcinoma. Next, we explored the regulatory mechanism of MUC1 in CSCC. MUC1 overexpression promoted the proliferation and metastasis abilities of cervical cancer cells. MUC1 could regulate ERK phosphorylation, then upregulated ITGA2 and ITGA3 expression. Further knockdown of ITGA2 and ITGA3 significantly inhibited tumorigenesis of cervical cancer cells. Moreover, we designed a combination drug regimen with MUC1-siRNA and ERK inhibitor in vivo, founding that the combination of drugs achieved better results in animals with xenograft compared with targeting MUC1 alone. Taken together, we discovered a novel regulatory MUC1/ERK/ITGA2/3 pathway in cervical cancer that may serve as potential biomarkers and therapeutic targets in the future.
Project description:Gastric cancer is a highly immunogenic malignancy. Immune tolerance facilitated by myeloid-derived suppressor cells (MDSCs) has been implicated in gastric cancer resistance mechanisms. The potential role of APE1 in regulating gastric cancer metastasis by targeting MDSCs remains uncertain. In this study, the plasmid Plxpsp-mGM-CSF was used to induce high expression of granulocyte-macrophage colony-stimulating factor (GM-CSF) in GES-1 cells. For tumor transplantation experiments, AGS, AGS+GM-CSF and AGS+GM-CSF-siAPE1 cell lines were established by transfection, followed by subcutaneous implantation of tumor cells. MDSCs, Treg cells, IgG, CD3 and CD8 levels were assessed. Transfection with siAPE1 significantly inhibited tumor growth compared to the AGS+GM-CSF group. APE1 gene knockdown modulated the immune system in gastric cancer mice, characterized by a decrease in MDSCs and an increase in Treg cells, IgG, CD3 and CD8. In addition, APE1 gene knockdown resulted in decreased levels of pro-MDSC cytokines (HGF, CCL5, IL-6, CCL12). Furthermore, APE1 gene knockdown inhibited proliferation, migration and invasion of AGS and MKN45 cells. AGS-GM-CSF cell transplantation increased MDSC levels and accelerated tumor growth, whereas APE1 knockdown reduced MDSC levels, inhibited tumor growth and attenuated inflammatory infiltration in gastric cancer tissues.
