Expression data from human Bladder cancer cell line J82 with control or overexpression of SQLE
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE231045 | GEO | 2024/04/28
REPOSITORIES: GEO
Similar Datasets
Project description:Expression data from human Bladder cancer cell line J82 with control or overexpression of SQLE
| PRJNA962967 | ENA
Project description:To uncover the dysregulated genes in BCa, we performed the RNA-seq to detect the gene expression levels in four BCa cells (5637, UMUC3, T24, and J82) and human immortalized urothelial cell SV-HUC-1. To search for the differentially expressed genes of for cell lines (5637, J82, UMUC3, and T24) compared to the normal cell line SV-HUC-1.
2024-04-28 | GSE231383 | GEO
Project description:Frankincense oil is prepared from aromatic hardened wood resin obtained by tapping Boswellia trees. For thousands of years, it has been important both socially and economically as an ingredient in incense and perfumes. Frankincense oil is a botanical oil distillate made from fermented plants that contains boswellic acid, a component known to have anti-neoplastic properties. We evaluated frankincense oil-induced cytotoxicity in bladder cancer cells. With a window of concentration, frankincense oil suppressed cell viability and induced cytotoxicity in bladder transitional carcinoma J82 cells but not normal bladder urothelial UROtsa cells immortalized with SV40 large T antigen. However, frankincense oil-induced J82 cell death did not result in DNA fragmentation. Microarray and bioinformatics analysis confirmed that frankincense oil activated cell cycle arrest, suppressed cell proliferation, and activated apoptosis in J82 cells through a series of potential pathways. These finding suggest that bladder cancer can be treated through intravesical administration of pharmaceutical agents similar to direct application on melanoma. 2E05 J82 cells were untreated or treated with a 1/1000 dilution of frankincense oil for 0.5, 1, 2, or 3 hours prior to RNA extraction.
2009-02-09 | E-GEOD-14002 | biostudies-arrayexpress
Project description:Frankincense oil is prepared from aromatic hardened wood resin obtained by tapping Boswellia trees. For thousands of years, it has been important both socially and economically as an ingredient in incense and perfumes. Frankincense oil is a botanical oil distillate made from fermented plants that contains boswellic acid, a component known to have anti-neoplastic properties. We evaluated frankincense oil-induced cytotoxicity in bladder cancer cells. With a window of concentration, frankincense oil suppressed cell viability and induced cytotoxicity in bladder transitional carcinoma J82 cells but not normal bladder urothelial UROtsa cells immortalized with SV40 large T antigen. However, frankincense oil-induced J82 cell death did not result in DNA fragmentation. Microarray and bioinformatics analysis confirmed that frankincense oil activated cell cycle arrest, suppressed cell proliferation, and activated apoptosis in J82 cells through a series of potential pathways. These finding suggest that bladder cancer can be treated through intravesical administration of pharmaceutical agents similar to direct application on melanoma.
2009-02-10 | GSE14002 | GEO
Project description:J82 is a urothelial carcinoma (bladder cancer) derived cultured cell line (see COSMIC https://cancer.sanger.ac.uk/cosmic/sample/overview?id=753566). The cultured cell line MDXC1 was derived from J82 xenograft tumors grown in SCID/BEIGE mice for 50 days using conventional methods of tumor excision, cell dissociation and growth in culture for 15 passages. MDXC1 was confirmed to be solely of human origin and pathogen-free. J82 and MDXC1 cells were compared for phenotypic changes in cancer-related genes associated with xenograft tumor growth. Experiments were included in the following larger study: Title: Autocrine signaling by receptor tyrosine kinases in urothelial carcinoma of the bladder. Authors: Young H. Lee, Molly M. Lee, Dinuka M. De Silva, Arpita Roy, Cara Wright, Tiffany Wong, Rene Costello, Oluwole Olaku, Robert L. Grubb III#, Piyush K. Agarwal, Andrea B. Apolo*+ Donald P. Bottaro* Affiliations: Urologic Oncology Branch and +Genitourinary Malignancies Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892 USA and #Department of Urology, Medical University of South Carolina, Charleston, South Carolina 29425 USA Abstract: Comprehensive characterizations of bladder cancer (BCa) have established molecular phenotype classes with distinct alterations and survival trends. Extending these studies within the tyrosine kinase (TK) family to identify disease drivers could improve our use of TK inhibitors to treat specific patient groups or individuals. We examined the expression distribution of TKs as a class (n = 89) in The Cancer Genome Atlas (TCGA) muscle invasive BCa data set (n >400). Patient profiles of potentially oncogenic alterations (overexpression and/or amplification) clustered TKs into 3 groups; alterations of group 1 and 3 TKs were associated with significantly worse patient survival relative to those without alterations. Many TK pathways induce epithelial-to-mesenchymal transition (EMT), which promotes tumor invasiveness and metastasis. Overexpression and/or amplification among 9 EMT transcriptional activators occurred in 43% of TCGA cases. Co-occurring alterations of TKs and EMT transcriptional activators involved most group 1 TKs; 24% of these events were associated with significantly worse patient survival. Co-occurring alterations of receptor TKs and their cognate ligands occurred in 16% of TCGA cases and several BCa-derived cell lines. Suppression of GAS6, MST1 or CSF1, or their respective receptors (AXL, MST1R and CSF1R), in BCa cell lines was associated with decreased receptor activation, cell migration, cell proliferation and anchorage independent cell growth. These studies reveal the patterns and prevalence of potentially oncogenic TK pathway-related alterations in BCa and identify specific alterations associated with reduced BCa patient survival. Detection of these features in BCa patients could better inform TK inhibitor use and improve clinical outcomes.
2021-07-28 | GSE156348 | GEO
Project description:Cholesterol is essential for membrane biogenesis, cell proliferation and differentiation. The role of cholesterol in cancer development and the regulation of cholesterol synthesis are still under active investigation. Here we show that under normal-sterol conditions，p53 directly represses the expression of SQLE, a rate-limiting and the first oxygenation enzyme in cholesterol synthesis，in a SREBP2-independent manner. Through transcriptional downregulation of SQLE, p53 represses cholesterol production in vivo and in vitro, leading to tumor growth suppression. Inhibition of SQLE using small interfering RNA (siRNA) or terbinafine (a SQLE inhibitor) reverses the increased cell proliferation caused by p53 deficiency. Conversely, SQLE overexpression or cholesterol addition promotes cell proliferation, particularly in p53 wild-type cells. More importantly, pharmacological inhibition or shRNA-mediated silencing of SQLE restricts nonalcoholic fatty liver disease (NAFLD) -induced liver tumorigenesis in p53 knockout mice. Therefore, our findings reveal a role for p53 in regulating SQLE and cholesterol biosynthesis, and further demonstrate that downregulation of SQLE is critical for p53-mediated tumor suppression.
2021-07-18 | GSE176112 | GEO
Project description:We profile gene expression upon circCDYL KD in HepG2 cells and in two bladder cancer cell lines J82 and UMUC3 as well as upon knockdown of the RNA binding proteins (RBP) GRWD1, IGF2BP1, and IGF2BP2 in J82 and UMUC3
2020-11-11 | GSE146726 | GEO
Project description:We profile gene expression upon circHIPK3 KD in two bladder cancer cell lines UMUC3 and J82
2021-10-01 | GSE148824 | GEO
Project description:In our study, we found that SQLE was critical to osteosarcoma progression. To identify the mechanism of SQLE in osteosarcoma, we conducted the RNA-seq analysis of SQLE knockdown in osteosarcoma cell line U2OS cells.
2024-12-16 | GSE245562 | GEO
Project description:Uropathogenic Escherichia coli (UPEC) are the most common cause of urinary tract infection (UTI). UPEC normally reside in the intestine, and during establishment of UTI, it undergoes metabolic adaptations, first to urine and then upon tissue invasion to the bladder cell interior. In order to understand these adaptations, we used quantitative proteomic profiling to characterize protein expression of UPEC strain UTI89 growing in human urine and when inside J82 bladder cells. In order to facilitate detection of UPEC proteins over the excess amount of eukaryotic proteins in bladder cells, we developed a method where proteins from UTI89 grown in MOPS and urine was spiked-in to enhance detection of bacterial proteins. More than 2000 E. coli proteins were detected. During growth in urine, proteins associated with iron acquisition and several amino acid uptake and biosynthesis systems, in particular arginine metabolism, were significantly upregulated. During growth in J82 cells, proteins related to iron uptake and arginine metabolisms were upregulated together with proteins involved in sulphur compound turnover. Results suggested that UPEC experience a richer environment in bladder cells compared to urine. There was no direct correlation between upregulated proteins and proteins reported to be essential for infections, showing that upregulation during growth does not signify that the proteins are essential for growth under a condition.
2022-06-09 | PXD032049 | Pride