Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1177344 | ENA |
REPOSITORIES: ENA
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Project description:Bladder cancer is mostly present in the form of urothelium carcinoma, causing over 150.000 deaths each year. Its histopathological classification as muscle invasive and non-muscle invasive is the most prominent aspect, affecting the prognosis and progression of this disease. In this study, we defined the active regulatory landscape of MIBC and NMIBC cell lines using H3K27ac-seq and used an integrative data approach to combine our findings with existing data. Our analysis revealed FRA1 and FLI1 as the two critical transcription factors differentially regulating MIBC regulatory landscape. Importantly, we show that FRA1 and FLI1 regulate the genes involved in epithelial cell migration and cell junction organization. Knock-down of FRA1 and FLI1 in MIBC revealed the downregulation of several EMT-related genes such as MAP4K4 and FLOT1. Further, ChIP-SICAP performed for FRA1 and FLI1 enabled us to infer chromatin binding partners of these two transcription factors and link this information with their target genes, providing a comprehensive regulatory circuit for the genes implicated in invasive ability of the bladder cancer cells. Finally, we show that knock-down of FRA1 and FLI1 results in statistically significant less migration of cells using IC-CHIP assays. Our results collectively highlight the role of these two transcription factors in invasive characteristics of bladder cancer in selection and design of targeted options for treatment of MIBC.
2023-02-20 | GSE213533 | GEO
Project description:Molecules interacting with CasL 2 (MICAL2) belongs to a three-member family of multi-domain flavoprotein monooxygenase enzymes that catalyze actin oxidation-reduction reactions destabilizing F-actin in cytoskeletal dynamics. MICAL2 is over-expressed, being a negative prognostic factor, in aggressive gastric, kidney, prostate, bladder, breast and endometrial human cancer. MICAL2 is expressed in cancer-associated neo-angiogenic capillaries. The study of MICAL2 knock-down in endothelial cells shed light on the transcriptional impact of the gene on endothelial cell biology. To explore the transcriptional impact of the lack of Mical2 in endothelial cells, we performed genome-wide expression profiling of Mical2 knock-down SVEC4-10 (ATTC CRL-2181) cells (M2KD). Reference cells were: Mical3 knock-down (M3KD), obtained with same strategy; untreated SVEC4-10 cells ((WT), and cells transduced with insert-free viral vector (empty).
2019-04-29 | GSE120494 | GEO
Project description:Knock down of FTO in cervical cancer cells
| PRJNA551671 | ENA
Project description:4T1 breast cancer cells: SPARC knock down vs. Control
| PRJNA327127 | ENA
Project description:Expression profiling of cervical cancer cells with IGF2R knock down
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Project description:Amplification and overexpression of the E2F3 gene at 6p22 in human bladder cancer is associated with increased tumour stage, grade and proliferation index, and in prostate cancer E2F3 overexpression is linked to tumour aggressiveness. We first used small interfering RNA technology to confirm the potential importance of E2F3 overexpression in bladder cancer development. Knockdown of E2F3 expression in bladder cells containing the 6p22 amplicon strongly reduced the extent of bromodeoxyuridine (BrdU) incorporation and the rate of cellular proliferation. In contrast, knockdown of CDKAL1/ FLJ20342, another proposed oncogene, from this amplicon had no effect. Expression cDNA microarray analysis on bladder cancer cells following E2F3 knockdown was then used to identify genes regulated by E2F3, leading to the identification of known E2F3 targets such as Cyclin A and CDC2 and novel targets including pituitary tumour transforming gene 1, Polo-like kinase 1 (PLK1) and Caveolin-2. For both bladder and prostate cancer, we have proposed that E2F3 protein overexpression may cooperate with removal of the E2F inhibitor retinoblastoma tumor suppressor protein (pRB) to drive cellular proliferation. In support of this model, we found that ectopic expression of E2F3a enhanced the BrdU incorporation, a marker of cellular proliferation rate, of prostate cancer DU145 cells, which lack pRB, but had no effect on the proliferation rate of PC3 prostate cancer cells that express wild-type pRB. BrdU incorporation in PC3 cells could, however, be increased by overexpressing E2F3a in cells depleted of pRB. When taken together, these observations indicate that E2F3 levels have a critical role in modifying cellular proliferation rate in human bladder and prostate cancer. Keywords: siRNA knock down
2006-10-28 | GSE6131 | GEO