Project description:Matrix metalloproteinases (MMPs) have been traditionally implicated in cancer progression because of their ability to degrade the extracellular matrix. However, some members of the MMP family have recently been identified as proteases with antitumor properties. Thus, it has been described that collagenase-2 (MMP-8) has a protective role in tumor and metastasis progression, but the molecular mechanisms underlying these effects are unknown. We show herein that Mmp8 expression causes a decrease in miR-21 levels that in turn leads to a reduction in tumor growth and lung metastasis formation by MDA-MB-231 (4175) breast cancer cells. By using both in vitro and in vivo models, we demonstrate that the mechanism responsible for these MMP-8 beneficial effects involves cleavage of decorin by MMP-8 and a subsequent reduction of transforming growth factor ? (TGF-?) signaling that controls miR-21 levels. In addition, miR-21 downregulation induced by MMP-8 increases the levels of tumor suppressors such as programmed cell death 4, which may also contribute to the decrease in tumor formation and metastasis of breast cancer cells overexpressing this metalloproteinase. These findings reveal a new signaling pathway for cancer regulation controlled by MMP-8, and contribute to clarify the molecular mechanisms by which tumor-defying proteases may exert their protective function in cancer and metastasis.
Project description:The cytokine Oncostatin M (OSM) promotes cancer progression by acting as central node for multicellular interactions between cancer cells and surrounding stromal cells. OSM is mainly secreted by myeloid cells and the oncostatin M receptor (OSMR) is expressed by cancer cells and cancer associated fibroblasts (CAFs), among others. To understand the effect of OSM in triple negative breast cancer cells, a small and well-annotated Clariom S gene microarray was performed in OSM-overexpressing (MDA-MB-231-hOSM) and control (MDA-MB-231-hC) MDA-MB-231 cells.
Project description:Dicer, RNase III endonuclease, is an essential enzyme in miRNA biogenesis that regulates target gene expression, and it has been reported that aberrant expressions of Dicer associate with the clinical outcomes of patients in various cancers. To explore the miRNA differencial expression regulated by Dicer in MDA-MB-231/E1A cells, the microarray profiling analysis was employed to conduct differentially expressed miRNAs in stable MDA-MB-231/vector, MDA-MB-231/E1A, and MDA-MB-231/E1A/shDicer cells.
Project description:To obtain an overview of the cellular functions regulated by ZNF217 signaling in breast-cancer cell lines, we performed global gene-expression profiling on MDA-MB-231-pcDNA6 and MDA-MB-231-ZNF217 cells
Project description:Purpose: DnaJ heat shock protein family (Hsp40) member C12 (DNAJC12) belongs to Hsp40/DnaJ protein family containing a J domain.The goal of this study is to compare the transcriptomic profiling change of MDA-MB-231 cells overexpressing DNAJC12 compared with MDA-MB-231 cells transfected with empty vector. Methods: 5×10^6 cells of each sample were collected, and total RNA was extracted using TRIZOL. After extraction, the RNA integrality was validated by Agilent 2100 bioanalyzer, and the qualified RNA was used to establish an RNA library, which was checked by quality control with Agilent 2100 bioanalyzer before sequencing. Transcriptome sequencing was achieved by Illumina Novaseq platform.
Project description:Identification of genes that are involved in self-seeding by comparing gene expression profiles between parental MDA-MB-231 cells and seeder cells (MDA-231-S1a and S1b) 2 replicates from each sample (parental MDA-MB-231, MDA-MB-231 S1a and MDA-MB-231 S1b) were analyzed
Project description:Dicer, RNase III endonuclease, is an essential enzyme in miRNA biogenesis that regulates target gene expression, and it has been reported that aberrant expressions of Dicer associate with the clinical outcomes of patients in various cancers. To explore the miRNA differencial expression regulated by Dicer in MDA-MB-231/E1A cells, the microarray profiling analysis was employed to conduct differentially expressed miRNAs in stable MDA-MB-231/vector, MDA-MB-231/E1A, and MDA-MB-231/E1A/shDicer cells. The four groups including vector control, E1A-expressing and Dicer knockdown in E1A-expressing MDA-MB-231 cells were harvested and RNA were isolated. Two independent experiments were performed for each group.
Project description:A comparison of gene expression profiles between control- and mascpin-overexpressing MDA-MB-231 cells was performed to investigate the role of cytoplasmic maspin in breast cancer progression. The data provides insight into the importance of cytoplasmic maspin in breast cancer progression.
Project description:To obtain an overview of the cellular functions regulated by ZNF217 signaling in breast-cancer cell lines, we performed global gene-expression profiling on MDA-MB-231-pcDNA6 and MDA-MB-231-ZNF217 cells Two independent cell-culture replicates from the total population of MDA-MB-231-pcDNA6 and MDA-MB-231-ZNF217 stable transfectants were used to generate total RNA. Total RNA was extracted from cell culture using a Qiagen RNA extraction kit and RNA quality was assessed using the BioAnalyzer 2100™ (Agilent Technologies). Complex probes were produced from these RNA, then hybridized to Human genome U133 Plus 2.0 array according to the manufacturer’s recommendations (Affymetrix).
Project description:Analysis of MDA-MB-231 breast cancer cells overexpressing lncRNA neuroblastoma associated transcript 1 (NBAT1). Results provide insight into the function of NBAT1 in breast cancer. NBAT1 overexpressed in breast cancer cells MDA-MB-231 compared to control (empty vector alone). Three replicates of each treatment were analyzed.