Transcriptional profile of CAOV2 ovarian cancer cells with TAZ silencing
Ontology highlight
ABSTRACT: We performed RNAseq to study the transcriptional changes of human CAOV2 ovarian cancer cells with or without TAZ silencing by siRNAs to understand the genetic determinants of ferroptosis response
Project description:We performed RNAseq to study the transcriptional changes of human CAOV2 ovarian cancer cells with or without YAP silencing by siRNAs to understand the genetic determinants of ferroptosis response
Project description:TAZ, also known as WWTR1, is the one of the effectors of Hippo pathway. With its paralog, YAP, TAZ promotes organ size growth as well as tumor metastasis. In human renal carcinoma cells, we found that TAZ-silencing induces resisntance toward erastin-induced ferroptosis. In this study, TAZ is silencing in clear cell carcinoma cell line RCC4 to elucidate the downstream targets that promotes the resistance toward erastin-induced ferroptosis.
Project description:RNA sequencing (RNAseq) of N/TERT2G keratinocytes transduced with pooled siRNAs targeting YAP1 and TAZ (WWTR1), or non-targeting control siRNA (siCon)
Project description:We performed RNAseq to study the transcriptional changes of human CAOV2 recurrent vs CAOV2 primary ovarian cancer cells to understand the genetic determinants of ferroptosis response
Project description:Transcriptome analysis of prostate cancer patient derived organoid DU145 cell line upon knockdown of YAP, TAZ, or YAP/TAZ mediated by siRNAs
Project description:TAZ is an important transcriptional co-activator involved in the HIPPO pathway that regulates cell growth, tumorigenesis and organ development and can play as a key mediator in other signaling pathways, such as MESH1-regulated pathways. MESH1 is the human ortholog of spoT that regulates sringent response in bacteria. MESH1 silencing inhibits cell proliferation and triggers a genome-wide transcriptional reprogramming as how spoT works in bacteria, among which TAZ is significantly down-regulated. Therefore, we aim to investigate how much TAZ contributes to the MESH1-regulated gene signature. We performed this microarray restoring TAZ level upon MESH1 silencing and measured the rescue effect. Overall, approximately 30% of the MESH1 regulated genes (up or down-regulated by siMESH1 by at least 2 folds) were rescued by the TAZ overexpression by at least 1.5 folds. Interestingly, a series of cell cycle related genes (RRM1, RRM2,CDK1 and CDC6) were rescued by TAZ restoration, suggesting that TAZ is an important mediator involved in the MESH1-regulated pathway to trigger the downstream tarnscriptomic reprogramming and cell proliferation inhibition. By understanding the mechanisms of MESH1 and its regulated pathways, we may disclose a new target for cancer therapy to regulate cancer cell growth. We used microarrays to detail the coverage of TAZ regulated genes downstream to MESH1 regulated gene signature in H1975 cells.
Project description:Transcriptome analysis of prostate cancer patient derived organoid MKS-PCa3 upon knockdown of FOSL1, YAP, TAZ, or YAP/TAZ mediated by siRNAs
Project description:The Hippo pathway plays a crucial in organ size control during development and tissue homeostasis in adult life. To examine a role for Hippo signaling in the intestinal epithelium, we analyzed gene expression patterns in the mouse intestinal epithelilum transfected with siRNAs or expression plasmids for shRNAs targeting the Hippo pathway effectors, YAP and TAZ. We performed two independent series of experiments (siGFP (n=3) vs siYAP/siTAZ (n=3), and shLacZ (n=1) vs shYAP/shTAZ (n=1)). Control siRNA (siGFP), YAP/TAZ siRNAs, or expression plasmids for control shRNA (shLacZ) or YAP/TAZ shRNAs were introduced into the mouse intestinal epithelium by the newly-developed in vivo transfection method. Four days after transfection, intestinal epithelial cells were isolated from the tissues and total RNA was extracted.