Project description:Recent findings show that EMT in cancer is dynamic and display a number of intermediate stages along the transition to obtain a high phenotypic and functional cellular plasticity. To comprehend transcriptional regulation among major EMT-transcription factors (EMT-TFs) along the EMT spectrum, we performed gene expression profiles of EMT-TFs (SNAI1/2, ZEB1/2, TWIST1) overexpressing epithelial (PEO1, OVCA420) and intermediate epithelial (OVCA429) ovarian cancer cell clones. Our results show that these factors generate an unidirectional repressive regulation in cells with epithelial phenotype (PEO1, OVCA420), whereas a bidirectional activation regulation in cells with intermediate epithelial phenotype (OVCA429). Microarray data analysis of these EMT-TFs overexpression clones revealed a distinct signature of gene expression for each phenotype and the overlapping gene set show a strong negative correlation with EMT scores, indicating that loss of this gene set is essential to trigger EMT.
Project description:Chemo-resistance to platinum such as cisplatin is critical in the treatment of ovarian cancer. Recent evidences have linked epithelial-mesenchymal transition (EMT) with the drug resistance as a contributing mechanism. The current study explored the connection between cellular responses to cisplatin with EMT in ovarian cancer. 46 ovarian carcinoma cell lines expression data with and without Cisplatin treatment.
Project description:The present study is aimed at detecting and measuring mRNA levels of genes involved in epithelial to mesenchymal transition (EMT) in biological samples, i.e. in peripheral blood samples of colorectal cancer (CRC) patients and healthy controls, to determine the presence of disease, its progression and risk of recurrence.
Project description:Mouse ovarian cancer cells lines were generated from primary tumor tissues, metastatic tumor tissues and in vitro cultured ovarian bursa cells. Gene transcripts from the whole genome were tested using WG6 microarray to compare gene expression level of cells lines with and without Epithelial to Mesenchymal Transition(EMT).
Project description:We showed that in response to chemotherapy, dying cancer cells can secrete spliceosomal components into the extracellular space. These therapy-induced secretomes enriched with spliceosomal components promote the chemoresistance of recipient tumor cells. We demonstrated that spliceosomal proteins SNU13 and SYNCRIP can relocalize from dying tumor cells to recipient tumor cells via extracellular vesicles. To investigate whether the increased abundance of splicing factors could be the reason for the acquisition of a more aggressive phenotype by tumor cells, we got SKOV3 cell lines stably overexpressing SYNCRIP or SNU13. These cell lines were more resistant to cisplatin compared to control cell line expressing empty vector. Next, to investigate how the therapy response is formed in tumor cells with and without overexpression of spliceosomal proteins SNU13 or SYNCRIP, we performed RNAseq analysis of these cells before and 24 hours after cisplatin treatment. Enrichement analyses showed that in response to cisplatin, genes associated with DNA repair and cell cycle regulation were upregulated in cancer cell lines overexpressing SYNCRIP or SNU13 compared with control cells. This study revealed previously unknown signaling molecules in the microenvironment of ovarian cancer that have potential clinical significance.
Project description:Mouse ovarian cancer cells lines were generated from primary tumor tissues, metastatic tumor tissues and in vitro cultured ovarian bursa cells. Gene transcripts from the whole genome were tested using WG6 microarray to compare gene expression level of cells lines with and without Epithelial to Mesenchymal Transition(EMT). Total RNAs were isolated from different cell lines with two time points for each cell line and compare the differentially expressed genes in cell lines with different biological characteristics.
Project description:Chemo-resistance to platinum such as cisplatin is critical in the treatment of ovarian cancer. Recent evidences have linked epithelial-mesenchymal transition (EMT) with the drug resistance as a contributing mechanism. The current study explored the connection between cellular responses to cisplatin with EMT in ovarian cancer.
Project description:Little is known about the role of miR-200s in the progression of ovarian cancer. In this study we overexpressed the miR-200c/141 cluster, the miR-200b/200a/429 cluster, or both clusters in two different murine ovarian cancer cell lines (ID8 and 28-2). As co-oeverexpression of both clusters provided the best miR-200 overexpression, we evaluated ID8 and 28-2 cells overexpressing both miR-200 clusters (ID8-200f and 28-2-200f) compared to empty vector control cells (ID8EV and 28-2EV). ID8-200f and 28-2-200f cells showed increased expression of several mesenchymal genes, decreased proliferation, decreased invasion and increased apoptosis compared to their respective controls. RNA sequencing of ID8EV, ID8-200f, 28-2EV and 28-2-200f cells revealed that overexpression of miR-200s primary regulated genes involved in epithelial mesenchymal transition EMT) and gene implicated in migration. Therefore, our work suggests that miR-200s can inhibit characteristics associated ovarian cancer progression (increased proliferation and invasion and promotion of EMT).