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Effects and Mechanisms of ACSL4 Induces Immunosuppression in Colorectal Cancer [T84 cells]

ABSTRACT: Effects and Mechanisms of ACSL4 Induces Immunosuppression in Colorectal Cancer [T84 cells]

PROVIDER: PRJNA1199921 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31758355_1.fastq.gz	Fastqsanger.gz
	SRR31758355_2.fastq.gz	Fastqsanger.gz
	SRR31758356_1.fastq.gz	Fastqsanger.gz
	SRR31758356_2.fastq.gz	Fastqsanger.gz
	SRR31758357_1.fastq.gz	Fastqsanger.gz

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Effects and Mechanisms of ACSL4 Induces Immunosuppression in Colorectal Cancer [T84 cells]

Project description:Analysis of ACSL4 gene knockout in human colorectal cancer cell line. These results confirm the role of the ACSL4 gene in colorectal cancer.

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Effects and Mechanisms of ACSL4 Induces Immunosuppression in Colorectal Cancer

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Project description:ACSL4 expression appears to be inversely associated with steroid hormone and growth factor receptor expression in breast cancer and positively correlated with an aggressive breast cancer phenotype. Neither MCF-7 nor SKBr3 cells normally express ACSL4, and when manipulated to do so, develop basal-like characteristics, including increased proliferation, migration and anchorage independent growth. We used an Affymetrix array platform to assess changes in individual gene expression as a function of conditional and stable expression of ACSL4 in MCF-7 and SKBr3 cells. In experiment 1, MCF-7 Tet-ON cells were transfected with ACSL4 cDNA and induced to express ACSL4 by addition of 1ug/ml of doxycycline (A) or vehicle (C) for 72 hours. Three controls (C) and three doxycycline-induced (A) samples were evaluated for gene expression. In experiment 2, MCF-7 cells were stably transfected with either an empty vector (C) or Lenti-ORF-ACSL4 (A). In experiment 3, SKBr3 cells were stably transfected with either an empty vector (C) or Lenti-ORF-ACSL4 (A).

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