Project description:We report the high-throughput profiling of histone modifications( H3K4me3 and H3K27ac) inTRIM11 knockdown and KDM5C knockdown MDA-MB-231 cells. we generated genome-wide chromatin-state maps of MDA-MB-231 cells.This study provides the localization of H3K4me3 and H3K27ac on chromatin in TRIM11 knockdown and KDM5C knockdown MDA-MB-231 cells.
Project description:To investigate the function of Neuropilin-1 (NRP-1) in breast cancer MDA-MB-231 cells. CRISPR-Cas9 gene editing was used to knockout (KO) the NRP-1 gene in MDA-MB-231 human triple-negative breast cancer cells. Differentially expressed genes (DEGs) were determined in NRP-1 KO and parental MDA-MB-231 cells using whole transcriptome next-generation sequencing.
Project description:We report the gene expression patterns in MDA-MB-231 (a line selected for low metastatic ability), MDA-MB-231-1833 (its bone-tropic metastatic derivative line), MDA-MB-231p27CK-DD (a phosphomimetic cell line), MDA-MB-231-1833shp27 (p27 knockdown cell line), MDA-MB-231-1833PF1502 (PI3K inhibitor treatment). It shows that the gene expression pattern are regulated in a p27 phosphorylation-dependent manner.
Project description:To identify BCBM-relevant lncRNAs, we assessed the expression profiles of lncRNAs in parental MDA-MB-231 (231-PAR) cells and isogenic brain metastatic cells (231-BRN), which were isolated from brain-seeking 231-PAR cells
Project description:To identify breast cancer metastasis-relevant circRNAs, we assessed the expression profiles of circRNAs in parental MDA-MB-231 (231-PAR) cells, isogenic brain metastatic cells (231-BM6), lung metastatic cells (LM2) and bone metastatic cells (1833), which were isolated from brain, lung or bone-seeking 231-PAR cells
Project description:This study examines the therapeutic plausibility of using universal methyl group donor S-adenosylmethionine (SAM) to block breast cancer development, growth, and metastasis. cancer. Anti-tumor and anti-metastatic activity of SAM was evaluated through a series of studies in vitro using two different human breast cancer cell lines and in vivo using a MDA-MB-231 xenograft model of breast cancer. The data shown in this array is obtained from control and SAM-treated MDA-MB-231 cell lines.
Project description:Heterogeneity in cancer gene expression is typically linked to genetic and epigenetic alterations, yet post-transcriptional regulation likely influences these patterns as well. However, the quantitative contribution of post-transcriptional mechanisms to cancer transcriptome dynamics remains unclear. Here, we systematically measured mRNA dynamics across diverse breast cancer models, revealing that mRNA stability significantly shapes gene expression variability. To decipher the regulatory grammar underlying these dynamics, we developed GreyHound, an interpretable multimodal deep-learning framework integrating RNA sequence features and RNA-binding protein (RBP) expression. GreyHound identified an extensive network of RBPs and their regulons underlying variations in mRNA stability. Among these, we uncovered a metastasis-suppressive regulatory axis centered on the RNA-binding protein RBMS3 and its post-transcriptional control of the redox regulator TXNIP. Functional and molecular analyses revealed that RBMS3 depletion resulted in targeted transcript destabilization, which was associated with poor clinical outcomes and enhanced metastatic potential in xenograft models. Using in vivo epistasis studies, we confirmed that RBMS3 regulation of TXNIP mRNA stability drives this metastasis-suppressive program. These findings position the RBMS3-TXNIP regulatory axis as a key post-transcriptional mechanism in breast cancer and illustrate how interpretable models of RNA dynamics can uncover hidden regulatory programs in disease.