Project description:The ovarian cancer biomarker HE4 has been shown to have multiple effects on ovarian cancer pathogenesis. In order to reveal gene regulation upstream of HE4 biological effects in ovarian cancer, HE4 was overexpressed in OVCAR8 wild type ovarian cancer cells and compared to null vector transfected cells. To gain a more comprehensive understanding of HE4 effects and elucidate similarities/differences between short-term HE4 exposure versus stable overexpression, we also compared untreated wild type cells with cells exposed to recombinant HE4 protein.
Project description:To characterize the mesothelial cell-mediated changes of gene expression in ovarian cancer cells, we performed RNA sequencing in OVCAR8 cells with and without mesothelial cell co-culture.
Project description:Gene expression analysis of pancreatic tumors from genetically engineered mice (Pdx-Cre;LSL-KRASG12D;TGFBRIIf/f) with depletion of aSMA+ or FAP+ cells. The pancreas tumors were harvested and analysed for gene expression profiles comparisons.
Project description:We used a functional small interfering RNA (siRNA) screen in ovarian cancer cells to identify 17β-hydroxysteroid dehydrogenase type 14 (HSD17B14) as a novel regulator of small EV secretion. We showed that the knockdown of HSD17B14 altered multiple gene expression in OVCAR8 cells.
Project description:In order to explore the effect of SF3B1 inhibitor, pladienolide B, on ovarian cancer cells, OVCAR8 cells were treated with DMSO or 2nM pladienolide B for 72h. Cells were collected and performed RNA sequencing.
Project description:FAP+ cells had been reported to be present only in healing wounds and at sites of tissue remodelling. We have found FAP+ cells in many normal tissues and aimed to investigate whether these cells were related or whether FAP is upregulated in response to an external stimulus on a variety of cells. Furthermore we wanted to investigate whether FAP+ cells are simply fibroblasts and so compared their transcriptomic profiles to that of a typical fibroblastic population, the murine embryonic fibroblast. FAP+ cells were sorted from two mesenchymal tissues, visceral adipose and skeletal muscle, and from an epithelial organ, the pancreas. These were compared to MEFs. Cells were isolated in duplicate experiments and these were analysed separately. These were compared to previously published publically available CD4+ T-cell subset data.
Project description:The antitumor activity of bromodomain inhibitors (BETi) has been demonstrated across numerous types of cancer. As such, these inhibitors are currently undergoing widespread clinical evaluation. However, predictive biomarkers allowing the stratification of tumors into responders and non-responders to BETi are lacking. Here, we show significant anti-proliferative effects of BETi in vitro and in vivo against aggressive SCCOHT1 ovarian cancer models lacking the SWI/SNF-related, SMARCA4 protein . Transcriptomic analysis revealed that exposure to BETi potently down-regulated the oncogenic receptor tyrosine kinase HER3 in SCCOHT1 but not in resistant OVCAR8 cells. Repression of this pathway is found to be an important determinant of response to BETi in cells harboring a loss of SMARCA4. Overall, we propose that BETi represent a rational therapeutic strategy in poor prognosis, SMARCA4 deficient cancers.