Project description:The transcriptional profile of MDA-MB-231 cells silenced for CYTOR (LINC00152, long intergenic non-protein coding RNA 152) was compared to LNA-control-treated MDA-MB-231 cells to identify potential CYTOR targets.
Project description:We report the genome-wide distribution of H2AS40Gc, H3K4me3, H3K27me3, and H3K36me3 in the breast cancer cell line MDA-MB-231 and the expression profile of MDA-MB-231 depleted S40-type H2A. We found that H2AS40Gc positively correlated with H3K27me3 and regulated the expression of genes related to proliferation and migration.
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:Mutant p53 can acquires oncogenic properties supporting tumor growth, metastases and chemoresistance, by reprogramming cancer cell transcriptome, proteome and metabolome. To investigate what is the gene expression network regulated by mutant p53, we silenced its expression in MDA-MB-231 Triple Negative Breast Cancer (TNBC) cell line. We then performed gene expression profiling analysis using data obtained from RNA-seq of MDA-MB 231.
Project description:Copy number gain/amplification of SETDB1 has been found in several human cancers, but the detailed oncogenic mechanism(s) of SETDB1 contributing to breast cancer remains largely unexplored. In this project, we analyzed the transcriptome of human breast cancer cell lines (MDA-MB-231 and MDA-MB-453) upon silencing of SETDB1 to explore the potential mechanism(s) underlying SETDB1 promoted breast cancer. In MDA-MB-231 cells, SETDB1 was silenced by shRNA-1. In MDA-MB-453 cells, SETDB1 was reduced by shRNA-3.
Project description:Aurora Kinase B and ZAK interaction model
Equivalent of the stochastic model used in "Network pharmacology model predicts combined Aurora B and ZAK inhibition in MDA-MB-231 breast cancer cells" by Tang et. al. 2018.
The only difference is cell division and partitioning of the components, which are available in the original model for SGNS2.
Project description:Mutant p53 can acquires oncogenic properties supporting tumor growth, metastases and chemoresistance, by reprogramming cancer cell transcriptome, proteome and metabolome. To investigate what is the gene expression network regulated by mutant p53 in condition of limited amino acids availability, we silenced mutant p53 expression in MDA-MB-231 Triple Negative Breast Cancer (TNBC) cell line, grown in medium with 100% and medium with 25% of amino acids. We performed gene expression profiling analysis using data obtained from RNA-seq of MDA-MB 231.
