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Transcriptional profile of CAOV2 ovarian cancer cells with TAZ silencing

ABSTRACT: Transcriptional profile of CAOV2 ovarian cancer cells with TAZ silencing

PROVIDER: PRJNA552107 | ENA |

REPOSITORIES: ENA

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Transcriptional profile of CAOV2 ovarian cancer cells with TAZ silencing

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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.

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TAZ overexpression partially rescued the transcriptomic reprogramming triggered by MESH1 silencing

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.

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