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Effects of kockouts of EGR1, FOS and their combination on the MAPK induced transcriptome [RNA_KO_clones]

ABSTRACT: Effects of kockouts of EGR1, FOS and their combination on the MAPK induced transcriptome [RNA_KO_clones]

PROVIDER: PRJNA1054484 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27292600.fastq.gz	Fastqsanger.gz
	SRR27292700.fastq.gz	Fastqsanger.gz
	SRR27292601.fastq.gz	Fastqsanger.gz
	SRR27292701.fastq.gz	Fastqsanger.gz
	SRR27292602.fastq.gz	Fastqsanger.gz

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Effects of kockouts of EGR1, FOS and their combination on the MAPK induced transcriptome [RNA_KO_clones]

Project description:In this study we used CRISPR/Cas9 to generate KO clones of the HEK-RAF-ER cell line that lack expression of EGR1, FOS and profiled the transcriptome after inducing RAF/MAPK signaling.

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Project description:Lung cancer is the main cause of cancer-related death in men and women all over the world. Lung adenocarcinoma (LUAD) is the most common histological subtype of lung cancer, with the overall 5-year survival rate is less than 20% . We found the mRNA expression of c-Fos in LUAD clinical samples was decreased significantly compared to adjacent normal control. Overexpression of c-Fos inhibited LUAD cell proliferation, colony formation, and induced cell apoptosis while c-Fos knockdown promoted cell proliferation, colony formation, and suppressed cell apoptosis. Cell cycle showed little difference after c-Fos knockdown but overexpression of c-Fos increased the distribution of G1 phase when decreased G2 phase cells. Knockdown of c-Fos reduced the sensitivity of LUAD cells to cisplatin but overexpression of c-Fos increased the efficacy of cisplatin both in vitro and in vivo. MAPK signaling pathway was enriched after c-Fos was overexpressed in LUAD cells. The expression of c-Jun, c-Myc and DUSP1 was greatly inhibited after c-Fos overexpression but incresed after c-Fos knockdown, which suggests c-Fos regulated MAPK signaling pathway in LUAD. Furthermore, c-Fos was shown to interact with c-Jun and overexpression of c-Jun partially recovered the expression of c-Jun, c-Myc and DUSP1 caused by c-Fos overexpression. Cell proliferation was also rescued when apoptosis was decreased followed by c-Jun overexpression. In contrast, knockdown of c-Jun inhibited cell proliferation and promoted cell apoptosis in LUAD cells when reduced the level of c-Jun, c-Myc and DUSP1. In summary, c-Fos inhibits cell proliferation, promotes apoptosis and increses cisplatin-sensitivity of lung adenocarcinoma cells via regulating MAPK signaling by interacting with c-Jun in certain LUADs.

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EGR1 regulation in human bone marrow stromal cells

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MAPK

Project description:MAPK

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