{"database":"ENA","file_versions":[],"scores":null,"additional":{"omics_type":["Genomics"],"center_name":["Biostatistics, Ducan Cancer Center, Baylor College of Medicine"],"full_dataset_link":["https://www.ebi.ac.uk/ena/browser/view/PRJNA224106"],"scientific_name":["Homo sapiens"],"long_description":["Prostate stroma-specific TGF-beta signaling induces morphological changes in LNCaP cells. We have previously shown that stromal TGF-beta signaling regulates prostate tumor growth. To further delineate the underlying mechanisms, we generated LNCaP cells overexpressing an HA-tagged constitutively activate TGF-beta1 ligand (LNCaP-HA-TGF-β1(a)) and control LNCaP cells (LNCaP-Ctrl), and performed in vitro co-cultures of LNCaP-HA-TGF-β1(a) and LNCaP-Ctrl cells on top of the confluent HPS-19I cells, a human prostate stromal cell line. Since LNCaP cells are defective in TGF-beta receptor I (TbetaRI / ALK-5) that is essential for mediating TGF-beta signaling, only HPS19I cells are able to respond to TGF-beta ligand in these co-cultures. This provides a unique opportunity to study how prostate stromal cell-specific TGF-beta signaling regulates PCa biology. To identify the prostate epithelia-specific gene that was regulated by prostate stromal TGF-beta signaling, we also treated HPS19I cells using conditioned media collected from LNCaP- HA-TGF-β1(a) cells and LNCaP-Ctrl cells cultured in RPMI1640 supplemented with 0.2% FBS. After 6 days of treatment, we extracted total RNA from these HPS19I cells and performed microarray. Overall design: HPS-19I prostate stroma cells from LNCaP+HPS-19I co-culture, with or without TGF-beta KEYWORDS: two group comparison"],"tag":["xref:PubMed:25333263"],"repository":["ENA"],"name_synonyms":["Human, Modern., human being, Man (Taxonomy), Homo sapiens, man, Man, human, Modern Man"],"description_synonyms":["signalling., hereditary prostate cancer, l(3)j5A5, cancer of the prostate, biological signaling, Cocultures, Coculture Technique, ho, Tgf-r, pun, TGF-b, Prostate Neoplasms, Punt, Neoplasms, M(2)LS1, familial, TGF-beta5, TGF-beta, Tg, Bone-Derived Transforming Growth Factor, AtrII, Act-r, CG9885, Factor, DPP-C, lap, Cell, CG7904, TGFbeta, Milk, Bone Derived Transforming Growth Factor, tgfbeta, Milk Growth Factor, Hin-d, Milk Growth, DmelCG9885, Atr88CD, Atr-II, l(2)22Fa, Prostatic Cancer, PUNT, DmelCG7904, Neoplasm, Prostatic Cancers, NOS, Cocultivation, Growth Factor, tgfb5, Cocultivations, l(3)10460, Cancer of Prostate, Co-culture, Prostate Cancers, Dm-DPP, l(2)k17036, shv, Coculture, ced, Dpp, DPP, transforming growth factor beta, Co-cultures, tgf-beta, M(2)23AB, l(2)10638, dlhC, Platelet Transforming Growth Factor, Cancers, tgfb, cancer of prostate, Prostate Neoplasm, blk, Prostatic Neoplasm, BMP, Cancer of the Prostate, signalling process, TGF-B, signaling process, Put, Prostatic, prostate cancer, atrII, PC, dpd1, Co culture, STK-C, Prostate Cancer, stromal connective tissue, Prostate, Atr, single organism signaling, Cancer"],"additional_accession":[]},"is_claimable":false,"name":"Homo sapiens","description":"Expression profiling of stroma cells from prostate cancer co-cultures, with or without TGF-beta signaling","dates":{"last_updated":"2025-09-24","first_public":"2014-11-13"},"accession":"PRJNA224106","cross_references":{"GEO":["GSE51622"],"taxon":["9606"],"PubMed":["25333263"]}}