{"database":"ENA","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Fastqsanger.gz":["ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR216/063/SRR21617363/SRR21617363_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR216/067/SRR21617367/SRR21617367_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR216/067/SRR21617367/SRR21617367_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR216/066/SRR21617366/SRR21617366_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR216/065/SRR21617365/SRR21617365_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR216/064/SRR21617364/SRR21617364_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR216/062/SRR21617362/SRR21617362_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR216/064/SRR21617364/SRR21617364_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR216/063/SRR21617363/SRR21617363_2.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR216/065/SRR21617365/SRR21617365_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR216/062/SRR21617362/SRR21617362_1.fastq.gz","ftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR216/066/SRR21617366/SRR21617366_2.fastq.gz"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Genomics"],"center_name":["Department of Thoracic Surgery"],"full_dataset_link":["https://www.ebi.ac.uk/ena/browser/view/PRJNA881720"],"scientific_name":["Homo sapiens"],"long_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. Overall design: mRNA profiles of SOX9 shRNA #1 vs. shCtrl & mRNA profiles of SOX9 shRNA #2 vs. shCtrl"],"repository":["ENA"],"additional_accession":[]},"is_claimable":false,"name":"c-Fos mediates cell proliferation, invasion and drug-resistance of lung adenocarcinoma through MAPK signal pathway","description":"c-Fos mediates cell proliferation, invasion and drug-resistance of lung adenocarcinoma through MAPK signal pathway","dates":{"last_updated":"2025-09-24","first_public":"2023-09-21"},"accession":"PRJNA881720","cross_references":{"GEO":["GSE213590"],"taxon":["9606"]}}