{"owner": "ArrayExpress Uploader", "ownerprofile_id": "arrayexpress_sid", "species": "mouse", "factors": [{"GSM560296": {"genotype": "wild type HIF2alpha"}}, {"GSM560296": {"genotype": "wild type HIF2alpha"}}, {"GSM560296": {"genotype": "wild type HIF2alpha"}}, {"GSM560296": {"genotype": "wild type HIF2alpha"}}, {"GSM560296": {"genotype": "wild type HIF2alpha"}}, {"GSM560296": {"genotype": "wild type HIF2alpha"}}, {"GSM560296": {"genotype": "wild type HIF2alpha"}}, {"GSM560303": {"genotype": "floxed HIF2alpha"}}, {"GSM560303": {"genotype": "floxed HIF2alpha"}}, {"GSM560303": {"genotype": "floxed HIF2alpha"}}, {"GSM560303": {"genotype": "floxed HIF2alpha"}}, {"GSM560303": {"genotype": "floxed HIF2alpha"}}, {"GSM560303": {"genotype": "floxed HIF2alpha"}}, {"GSM560303": {"genotype": "floxed HIF2alpha"}}], "id": 8489, "pop_total": 0, "platform": 8, "summary_wrapped": "Non-small cell lung cancer (NSCLC) is the leading cause of cancer deaths worldwide.  The oxygen-sensitive Hypoxia Inducible Factor (HIF)...", "geo_gse_id": "E-GEOD-22575", "owner_profile": "/profile/8773/arrayexpressuploader", "factor_count": 1, "sample_count": 14, "tags": ["cancer", "cell", "lung", "lung cancer", "nsclc"], "lastmodified": "Dec.12, 2014", "is_default": false, "geo_id_plat": "E-GEOD-22575_A-AFFY-36", "slug": "transcription-profiling-by-array-of-non-small-cell", "geo_gds_id": "", "name": "Transcription profiling by array of non-small cell lunch tumors from mice with floxed HIF2alpha", "created": "Nov.24, 2014", "summary": "Non-small cell lung cancer (NSCLC) is the leading cause of cancer deaths worldwide.  The oxygen-sensitive Hypoxia Inducible Factor (HIF) transcriptional regulators HIF-1\u03b1 and HIF-2\u03b1 are overexpressed in many human NSCLCs, and constitutive HIF-2\u03b1 activity can promote murine lung tumor progression, suggesting that HIF proteins may be effective NSCLC therapeutic targets. To investigate the consequences of inhibiting HIF activity in lung cancers, we deleted Hif-1\u03b1 or Hif-2\u03b1 in an established KrasG12D-driven murine NSCLC model.  Deletion of Hif-1\u03b1 had no obvious effect on tumor growth, whereas Hif-2\u03b1 deletion resulted in an unexpected increase in tumor burden that correlated with reduced expression of the candidate tumor suppressor gene Scgb3a1 (HIN-1). Here, we identify Scgb3a1 as a direct HIF-2\u03b1 target gene, and demonstrate that HIF-2\u03b1 regulates Scgb3a1 expression and tumor formation in human KrasG12D-driven NSCLC cells.  AKT pathway activity, reported to be repressed by Scgb3a1, was enhanced in HIF-2\u03b1 deficient human NSCLC cells and xenografts.  Finally, a direct correlation between HIF-2\u03b1 and SCGB3a1 expression was observed in approximately 70% of human NSCLC samples analyzed. These data suggest that whereas HIF-2\u03b1 overexpression can contribute to NSCLC progression, therapeutic inhibition of HIF-2\u03b1 below a critical threshold may paradoxically promote tumor growth by reducing expression of tumor suppressor genes, including Scgb3a1. RNA was isolated from tumors of experimental (Hif2alpha deficient) mice and control mice (seven for each group).", "source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-22575", "sample_source": "http://www.ebi.ac.uk/arrayexpress/experiments/E-GEOD-22575/samples/"}