Project description:Expression of the membrane glycoprotein podoplanin is upregulated in several human cancers and might be associated with their malignant progression. The exact biological function and molecular targets of cancer cell-expressed podoplanin have remained unclear, however. Here, we ectopically overexpressed podoplanin in a human breast carcinoma xenograft model to study its role in cancer progression. To identify molecular mediators of podoplanin-induced effects we compared transcriptional profiles of podoplanin-overexpressing and control tumors. Keywords: comparative transcriptional profiling
Project description:Expression of the membrane glycoprotein podoplanin is upregulated in several human cancers and might be associated with their malignant progression. The exact biological function and molecular targets of cancer cell-expressed podoplanin have remained unclear, however. Here, we ectopically overexpressed podoplanin in a human breast carcinoma xenograft model to study its role in cancer progression. To identify potential molecular mediators of podoplanin-induced effects in the murine tumor stroma we compared transcriptional profiles of podoplanin-overexpressing and control tumors using mouse microarrays. Keywords: comparative transcriptional profiling
Project description:To explore the potential target lncRNAs of EZH2 in breast cancer cells, we determined the lncRNA expression profiles in MCF7-control and MCF7-EZH2 overexpressing cells using lncRNA Microarray.
Project description:The goal of this study is to identify ERalpha-target genes affected by overexpression of the histone arginine methyltransferase CARM1 in breast cancer cells. The roles of CARM1 in ERalpha+ breast cancer was not well characterized. Therefore, we created a Dox inducible CARM1 overexpressing MCF7 cell line where CARM1 is overexpressed by 2 fold to determine the created a Dox-inducible CARM1 overexpressing MCF7 cells for evaluation of the global effects of CARM1 on Eralpha-target gene expression.
Project description:The goal of this study is to identify ERalpha-target genes affected by knocking down of the histone arginine methyltransferase CARM1 in MCF7 breast cancer cells. The roles of CARM1 in ERalpha+ breast cancer was not well characterized. Therefore, we created a Dox inducible CARM1 knockingdown MCF7 cell line where CARM1 is decreased to 20% of endogeneous level to determine the created a Dox-inducible CARM1shRNA overexpressing MCF7 cells for evaluation of the global effects of CARM1 on ERalpha-target gene expression.
Project description:To identify the microRNA-27b (miR-27b) target genes in luminal-type breast cancer cells, we performed the microarray analysis using miR-27b knockdown MCF7-luc cell line (MCF7-luc anti-miR-27b), miR-27b overexpressing MCF7-luc cell line (MCF7-luc miR-27b o.e.) and their contro cell line (MCF7-luc anti-NC).
Project description:The goal of this study is to identify ERalpha-target genes affected by overexpression of the histone arginine methyltransferase CARM1 in breast cancer cells. The roles of CARM1 in ERalpha+ breast cancer was not well characterized. Therefore, we created a Dox inducible CARM1 overexpressing MCF7 cell line where CARM1 is overexpressed by 2 fold to determine the created a Dox-inducible CARM1 overexpressing MCF7 cells for evaluation of the global effects of CARM1 on Eralpha-target gene expression. MCF7-tet-on-CARM1 clone 13 were treated under 4 conditions: DMSO; Dox; E2 (10nM); Dox+E2. In Dox+E2 condition, cells were pre-treated with Dox for 5 days before treating with E2 for 4 hours. 3 biological replicates were included and total of 12 samples were analyzed.
Project description:The SLC22A18 gene, which encodes an orphan transporter, is located at the 11p15.5 imprinted region, an important tumor-suppressor gene region. However, the role of SLC22A18 in tumor suppression remains unclear. Here, we investigated the involvement of SLC22A18 in cell growth, invasion and drug resistance of MCF7 human breast cancer cell line. Western blot analysis indicated that SLC22A18 is predominantly expressed at intracellular organelle membranes. Quantitative proteomics showed that knockdown of SLC22A18 significantly altered the expression of 578 (31.0%) out of 1867 proteins identified, including proteins related to malignancy and poor prognosis of breast cancer.
