Ontology highlight
ABSTRACT:
PROVIDER: PRJNA824993 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18693283.fastq.gz | Fastqsanger.gz | |||
| SRR18693284.fastq.gz | Fastqsanger.gz |
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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.
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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.
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Project description:Cigarette smoke has been demonstrated to stimulate the growth of existing bladder tumors by enhancing the survival and proliferation of cancer cells through the action of carcinogens present in smoke. Concurrently, Fatty Acid Synthase (FASN), a key enzyme in fatty acid synthesis crucial for lipid metabolism, exhibits dysregulation in various cancer types, often correlating with aggressive phenotypes. In this study, we reveal altered fatty acid metabolism and elevated FASN and fatty acid levels, specifically in current smokers with bladder cancer (BLCA). Notably, increased FASN levels under smoke exposure are attributed to epigenetic alterations affecting fatty acid metabolism. Cells exposed to cigarette smoke demonstrate a metabolic shift in utilizing glutamine as a carbon source and producing fatty acids. The genetic and pharmacological inhibition of FASN effectively reduces tumor growth in a CAM model exposed to smoke. FASN inhibitors like TVB 2640, currently in phase II clinical trialsclinical trials in various cancer types, may be effective for smokers with BLCA exhibiting high FASN levels. In general, FASN inhibition offers therapeutic promise for mitigating the impact of cigarette smoke on bladder cancer progression.
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