Project description:Background: We searched triple negative breast cancer (TNBC) specifically expressing candidates for target therapy. Methods: High expressing genes in three TNBC cell lines compared to three non-TNBC cell lines were evaluated by using RNA sequencing (log2 ratio>5, q<0.05). By integrating the shRNA library screening and public gene expression databases, we identifyied candidates for therapeutic targets. The expression significance of the candidates was examined by using immunohistochemistry of 248 clinical breast cancer patients. Results: One hundred seventy one genes were detected as highly expressed genes in TNBC cell lines than non-TNBC cell lines, and 13 genes were picked up as candidates not expressing in non-cancerous tissues. Integrated analysis with shRNA screening identified three candidates as TBNC specific molecular targets. Protein staining were stronger in breast cancer tissues, especially TNBC, than in the normal tissues.
Project description:We used MYOSIN10 shRNA to stably silence the expression of endogenous MYOSIN10 in Breast cancer cell MDA-MB-231. To investigate the inner change of cells with silenced MYOSIN10, we conducted a genome-wide screening for all potential genes affected by MYOSIN10 shRNA using Affymetrix Human Genome U133 plus 2.0 array. We showed genes affected by MYOSIN10 knockdown in breast cancer cell MDA-MB-231
Project description:Background: We searched triple negative breast cancer (TNBC) specifically expressing candidates for target therapy. Methods: High expressing genes in three TNBC cell lines compared to three non-TNBC cell lines were evaluated by using RNA sequencing (log2 ratio>5, q<0.05). By integrating the shRNA library screening and public gene expression databases, we identifyied candidates for therapeutic targets. The expression significance of the candidates was examined by using immunohistochemistry of 248 clinical breast cancer patients. Results: One hundred seventy one genes were detected as highly expressed genes in TNBC cell lines than non-TNBC cell lines, and 13 genes were picked up as candidates not expressing in non-cancerous tissues. Integrated analysis with shRNA screening identified three candidates as TBNC specific molecular targets. Protein staining were stronger in breast cancer tissues, especially TNBC, than in the normal tissues.
Project description:We identified quinolinate phosphoribosyltransferase (QPRT) as a prognostic factor in breast cancer. Transcription profiling analysis was performed in breast cancer cells transfected with control or QPRT shRNA.
Project description:Analysis of the effect of shRNA-mediated knockdown of SOX4 on global gene expression levels in MDA-MB-231 human breast cancer cells. Results were used for the identification of overlapping up- and downregulated genes in TRPM7 + SOX4 shRNA MDA-MB-231 cells
Project description:Frequent loss of heterozygosity (LOH) at 11q22-23 in breast cancer strongly suggests that this region contains a tumor suppressor gene, yet to be identified. We and others have shown Yes-associated protein (YAP), which is located at 11q22.2, transactivates the p53 family member p73 upon DNA damage, suggesting a tumor suppressive function for YAP. Our analysis of breast tumor tissues by immunohistochemistry (IHC) showed loss of YAP protein expression in great portion of breast cancers. We used microarray to look at the targte genes regulated by YAP in normal breast luminal cell and breast cancer cell lines. Experiment Overall Design: We generated stable cell lines by introducing control vector(pRS-IRES-GFP/pmig) or YAP shRNA(pRS-IRES-GFP-YAP/pmig-YAP) in a normal breast luminal cell line 1089 luminal and breast cancer cell lines MDA MB231. RAN was extracted and hybridized on Affymetrix microarrays.We looked for new target genes regulated by YAP in normal breast luminal cell and breast cancer cell lines.
Project description:DCD is a gene amplified and overexpressed in a subset of breast tumors acting as a growth and survival factor. Patients with DCD-positive breast cancer have worse prognostic features. To investigate the role of DCD in breast tumorigenesis, we analyzed the consequences of its downregulation in human breast cancer cell lines using three specific shRNA lentivirus vectors. Genes up- and down-regulated by DCD were identified using Affymetrix microarray and analyzed by MetaCore Platform. We found that loss of DCD expression led to reduced cell proliferation, resistance to apoptosis, and suppressed tumorigenesis in immunodeficient mice. Network analysis of gene expression data revealed perturbed ERBB signaling following DCD shRNA expression including changes in the expression of ERBB receptors and their ligands. These findings imply that DCD promotes breast tumorigenesis via modulating the activity of the ERBB signaling pathways. As ERBB signaling is also important for neural survival, HER2+ breast tumors may highjack DCD’s neural survival-promoting functions to promote tumorigenesis.