Project description:To investigate the mechanism through which miR-203 inhibited the breast cancer cell invasion, we overpression miR-203 in MDA-MB-231 cell line and performed a microarray to examine the genes which maybe targeted and down-regulated by miR-203.
Project description:To investigate the mechanism through which miR-203 inhibited the breast cancer cell invasion, we overpression miR-203 in MDA-MB-231 cell line and performed a microarray to examine the genes which maybe targeted and down-regulated by miR-203. We made a stable cell line(MB231/miR-203) which overexpressing miR-203 and a control cell line (MB231/EV) which expressing a contrlol vector. Total RNA were extracted from these two cell lines and subject to microarray.
Project description:Proteomic analysis of differentially expressed proteins in MDA-MB-231 and MCF-10A cell lines when miR-200c and miR-203 were transiently expressed or inhibited, respectively.
Project description:This study identifies miR-138 as a prognostic biomarker for basal breast carcinoma. Identification of differentially regulated genes upon miR-138 knockdown (AntagomiR-138) in basal breast cancer cell lines MDA-MB-231
Project description:MiR-200c is a well-studied miRNA that is involved in stemness, the epithelial-mesenchymal transition, chemoresistance, radioresistance, and invasion/metastasis of various cancer cells. To obtain an overview of the lncRNA/mRNA regulated by miR-200c signaling in breast-cancer cell lines, we performed global lncRNA/mRNA-expression profiling on MDA-MB-231-pGIPZ and MDA-MB-231-miR-200c cells.
Project description:the LM2 breast cancer cell line is an in vivo derived line from the MDA-MB-231 parental line. this LM2 line has been transduced either with a short hairpin control or miR-335 expression vector. Keywords: breast cancer, metastasis, miRNA
Project description:As miR-210 expression is correlated to poor prognosis both in estrogen-positive and in estrogen-negative breast cancer (BC) patients, we aimed to investigate the biological processes regulated by miR-210 and which may elucidate its function in the aggressive phenotype of high grade breast cancer. We performed in silico functional analyses of the genes deregulated upon miR-210 overexpression in MCF7 BC cell line and upon miR-210 repression in MDA-MB-231 BC cell line using lentiviral transduction. Gene expression profiling analysis of these cells revealed the deregulation of genes involved in several biological pathways including cell adhesion, extracellular structure organization, epithelial cell proliferation, cell division, cell cycle and immune response. MCF-7 cells overexpressing miR-210 (or control) and MDA-MB-231 cells in which miR-210 (or control) is repressed were used for RNA extraction and hybridization on Affymetrix microarrays.
Project description:To investigate the effects of breast cancer derived EVs on liver metabolism,we inoculated MDA-MB-231,231 /Rab27A KD and 231 /miR-9 KO cells into subcutaneous tumor in NSG mice. We then performed gene expression profiling analysis using data obtained from RNA-seq of liver from mice xenografted MDA-MB-231 cells (tumor bearing) or MDA-MB-231/Rab27A KD cells (231/Rab27A KD) or MDA-MB-231 /miR-9 KO (231/miR-9 KO) and tumor free mice.
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: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.
