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Comparison of gene expression profiles between SCD1/FADS2 knockdown and vector control of ovarian cancer cells OVCA433 by RNA-sequencing

ABSTRACT: Comparison of gene expression profiles between SCD1/FADS2 knockdown and vector control of ovarian cancer cells OVCA433 by RNA-sequencing

PROVIDER: PRJNA713769 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13937774_1.fastq.gz	Fastqsanger.gz
	SRR13937774_2.fastq.gz	Fastqsanger.gz
	SRR13937775_1.fastq.gz	Fastqsanger.gz
	SRR13937775_2.fastq.gz	Fastqsanger.gz
	SRR13937776_1.fastq.gz	Fastqsanger.gz

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Comparison of gene expression profiles between SCD1/FADS2 knockdown and vector control of ovarian cancer cells OVCA433 by RNA-sequencing

Project description:To understand the dependence of ovarian tumor cells on fatty acid metabolism, we performed transcriptome analysis using OVCA433 ovarian cancer cells, in which SCD1/FADS2 was genetically ablated via CRISPER/Cas9.

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Project description:Niche for stem cells can profoundly influence the position and fate of stem cells in tissue homeostasis and associated disorders, however, the mechanisms underlying the maintenance of stem cell niche remain poorly understood. Here we report that fatty acid desaturation catabolized by stearoyl-coenzyme A desaturase 1 (SCD1) regulates the activity of hair follicle stem cells (HFSCs) via blocking the formation of the bulge, a niche for HFSCs. We further unraveled that the abnormal hair growth in mice with SCD1 deletion is due to its function in K14+ basal keratinocytes rather than directly affecting HFSCs. Mechanistically, SCD1 deficiency impaired the expression of integrin α6 and the formation of hemidesmosomes (HDs), and thus allowed the activation of FAK in K14+ keratinocytes. Activated FAK subsequently stimulated PI3K and promoted the differentiation and proliferation of these keratinocytes, resulting in downward extension of the outer root sheath (ORS) and the disruption of bulge formation. Interestingly, inhibition of PI3K signaling restored bulge formation and normalized HFSCs and hair growth. Supplementation of oleic acid, the product of SCD1, to SCD1-/- mice also enhanced HD numbers, normalized the niche of HFSCs, and promoted hair growth in SCD1-/- mice. Taken together, SCD1 is indispensable for hair growth through stabilizing the number of HDs and thus sustaining bulge formation for HFSC residence and periodic activity.

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Project description:Presently, there is a deficiency of effective therapies designed to target clear cell renal cell carcinoma (ccRCC), with poor prognosis resulting in patients with advanced disease. Additionally, there is a lack of molecular factors which can be remedially targeted resulting in tumor specific inhibition, and therefore current therapeutic approaches often produce adverse side effects in patients. We identified that Stearoyl-CoA desaturase 1 (SCD1) was consistently overexpressed in patient ccRCC samples, and further investigation of SCD1 as a potential molecular target for ccRCC intervention utilizing a SCD1 inhibitor (A939572) resulted in tumor specific growth inhibition and induction of cell death. In order to understand the mechanism by which the SCD1 inhibitor mediated its anti-tumor effects, we performed gene array analysis and compared expression patterns between treated and untreated samples. Four established ccRCC cell lines purchased from ATCC were treated with DMSO control versus A939572 over a 24 hour time period. RNA from each group was isolated and sent of for gene array anaylsis. Gene expression data from each individual treatment group was normalized to its respective DMSO contol, and resulting expression patterns associated with drug exposure was compared between the four cell lines.

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