Project description:VGLL3 promotes the expression of collagens in cardiac myofibroblasts Fibrosis is occurred various organs and there has been reported that fibrosis contributes about 45% of all mortalities in the developed countries. In fibrosis, extracellular matrix such as collagens is mainly produced by myofibroblasts. In this time, we knocked down VGLL3 in cardiac myofibroblasts by using siRNA.
Project description:Myofibroblasts are one of the key cell types in cardiac injuries, leading to scar tissue formation and reduced heart function. To investigate the impact of microcurrent treatment on these cells, primary rat cardiac fibroblasts were initially differentiated into myofibroblasts. Subsequently, the differentiated myofibroblasts were subjected to microcurrent treatment at 1 and 2 µA/cm2 direct current (DC) with and without polarity reversal. Microcurrent treatments resulted in distinct transcriptional signatures and improved cell behavior. The observations show signs of microcurrent-mediated reversal of myofibroblast phenotype, possibly reducing cardiac fibrosis, and providing insights for cardiac tissue repair.
Project description:To understand global expression changes in a knockdown of PGC1alpha (siPGC1alpha) vs control (siControl) in a lung metastatic cell line (4175) Metabolic adaptations play a key role in fuelling tumour growth. However, less is known regarding the metabolic changes that promote cancer progression to metastatic disease. Herein, we reveal that PGC-1a expression and activity are differentially regulated depending on breast cancer metastatic sites. Breast cancer cells that preferentially metastasize to lung display striking upregulation of PGC-1a expression. PGC-1a promotes breast cancer cell migration and invasion in vitro and augments lung metastasis in vivo. MDA-MB-231 lung variant (4175) cells were treated with a short interfering RNA (siRNA) for human PGC-1a (PPARG1A) or control siRNA for 48hrs 24 hours post-plating cells.
Project description:Co-treatment with soluble CD74 and MIF induced necroptosis in cardiac myofibroblasts. The underlying mechanism of sCD74/MIF-induced necroptosis are still unkown. We used a microarray to identify pathways regulated by co-treatment with sCD74 and MIF .
Project description:All samples are conditioned media from primary cultured human gastric myofibroblasts, derived from either carcinoma tissue, or adjacent non cancerous tissue. In each experiment the cancer-derived myofibroblasts are compared against the non-cancer derived myofibroblasts from the same patient. All of the experiments were samples from Patient 1, except for 648, which is from Patient 2. SILAC labelling in each case is; 567 - Methionine COFRADIC; Cancer-derived = Heavy, Non-cancer = Light 575 - N-terminal COFRADIC; Cancer-derived = Heavy, Non-cancer = Light 646 - Cancer-derived = Light, Non-cancer = Heavy 647 - Non-cancer = Heavy, Non-cancer = Light (same cell line labelled twice to create a control experiment) 648 - Cancer-derived = Heavy, Non-cancer = Light
Project description:To examine the role of CPNE8 and BHLHE41 in ovarian cancer cells, RMG1 cells were treated with siRNA targeting CPNE8 (siCPNE8 #A and #B) or control siRNA (siControl), and OVCAR3 cells were treated with siRNA targeting BHLHE41 (siBHLHE41 #A and #B) or control siRNA (siControl). Microarray analysis showed that CPNE8 and BHLHE41 are involved in cellular signaling pathways in ovarian cancer.
Project description:Cancer-associated fibroblasts are a major component of the cancer stroma. Here we focus on gastric cancer associated myofibroblasts (CAMs). CAMs secrete factors that increase the migration, invasion and proliferation of cancer cells when compared to adjacent tissue myofibroblasts (ATMs), or normal tissue myofibroblasts (NTMs). In this study we identified and quantified the proteins secreted by normoxic (21% O2) and hypoxic (1% O2) myofibroblast cells.