Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA224106 | ENA |
REPOSITORIES: ENA
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Project description:Co-cultures of prostate cancer cells and stroma cells, with or without TGF-beta signaling
| PRJNA224103 | ENA
Project description:Expression profiling of co-cultures of prostate cancer cells and stroma cells, with or without TGF-beta signaling
| PRJNA224104 | ENA
Project 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.
2014-11-12 | GSE51617 | GEO
Project 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.
2014-11-12 | GSE51622 | GEO
Project description:Calcitriol and transforming growth factors beta (TGF-β) are involved in several biological pathways such as cell proliferation, differentiation, migration and invasion. Their cellular effects could be similar or opposite depending on the genetic target, cell type and context. Despite the reported association of calcitriol deficiency and disruption of the TGF-β pathway in prostate cancer and the well-known independent effects of calcitriol and TGF-βs on cancer cells, there is limited information regarding the cellular effects of calcitriol and TGF-β in combination. In this study, we in vitro analyze the combinatory effects of calcitriol and TGF-β on cell growth and apoptosis using PC-3 and DU145 human prostate cancer cell lines. Using high-throughput microarray profiling of PC-3 cells upon independent and combinatory treatments, we identified distinct transcriptional landscapes of each intervention, with a higher effect established by the combinatorial treatment, following by TGF-β1 and later by calcitriol. A set of genes and enriched pathways converge among the treatments, mainly between the combinatory scheme and TGF-β1, but the majority were treatment-specific. Of note, CYP24A1, IGFBP3, SERPINE1, CDKN1A, NOX4 and UBE2D3 were significantly up-regulated upon the combinatorial treatment whereas CCNA1, members of the CT45A and APOBEC3 family were down-regulated. By public RNA signatures, we were able to confirm the regulation by the co-treatment over cell proliferation and cell cycle. We finally investigated the possible clinical impact of genes modulated by the combinatorial treatment using benchmark prostate cancer data. This comprehensive analysis reveals that the combinatory treatment impairs cell growth without affecting apoptosis and their combinatory actions might synergize and improved their individual effects to reprogram prostate cancer signaling.
2020-12-15 | GSE159116 | GEO
Project description:The fibroblast growth factor receptor (FGFR) and canonical Wnt signaling pathways are important regulators of carcinogenesis; however, the interaction between these two pathways in the context of prostate cancer (PCa) has not been fully elucidated. Using novel transgenic mouse models, we describe Wnt-induced synergistic acceleration of FGFR1-driven adenocarcinoma; largely due to pronounced fibroblastic reactive stroma (RS) activation surrounding prostatic intraepithelial neoplasia (PIN) lesions in endogenous and reconstitution assays. Finally, both mouse and human RS are characterized by increases in TGF-β signaling heterogeneity immediately adjacent to PIN lesions; however, heterogeneity is lost during later stages of progression, likely contributing to tissue invasion. These studies confirm the importance of the FGFR1-Wnt-TGF-β signaling axes as driving forces behind reactive stroma and aggressive adenocarcinoma.
2014-01-07 | GSE41344 | GEO
Project description:The tumor microenvironment (TME) actively contributes to pancreatic ductal adenocarcinoma (PDAC) pathogenesis via a dynamic bidirectional tumor–stroma dialog. Here, we show that homologous recombination-defective (HRD) neoplastic epithelium reprograms its TME in a genotype-specific manner to promote cancer aggressiveness. Autochthonous mouse models, co-culture systems, and human PDAC specimens revealed that tumoral ATM serine/threonine kinase status impacts cancer-associated fibroblast fate towards αSMA+ myofibroblastic (myCAF) differentiation, while P53 operates mostly tumor cell intrinsic. Vice versa, myCAFs foster cancer aggressiveness and specific chemoresistance patterns. Secretomics, proteomics, and in vitro approaches uncovered a greater TGF-β1 release in ATM-deficient cells associated with an enhanced reactive oxygen species/actomyosin-mediated mechanism. Pharmacological interference with TGF-β signaling reverts myofibroblast differentiation, chemoresistance, and tumor promotion in various ATM-deficient PDAC models. Overall, our findings demonstrate specific TME reprogramming by HRD PDACs towards a cancer-promoting fate, and their eligibility for combinatorial therapies targeting intrinsic vulnerabilities and extrinsic tumor–stroma oncogenic crosstalks.
2026-04-27 | PXD042750 | Pride
Project description:We checked whether the inhibition of the FGF, VEGF, and TGF signaling pathways would influence the miRNA profile in ECs, co-cultured with NSPCs. EC/NSPC co-cultures were incubated with FGF/VEGF receptor inhibitor PD 173074 (1μM in DMSO), and the TGF-β receptor inhibitor SB431542 (10μM in DMSO, Millipore)
2012-01-01 | E-GEOD-32352 | biostudies-arrayexpress
Project description:The fibroblast growth factor receptor (FGFR) and canonical Wnt signaling pathways are important regulators of carcinogenesis; however, the interaction between these two pathways in the context of prostate cancer (PCa) has not been fully elucidated. Using novel transgenic mouse models, we describe Wnt-induced synergistic acceleration of FGFR1-driven adenocarcinoma; largely due to pronounced fibroblastic reactive stroma (RS) activation surrounding prostatic intraepithelial neoplasia (PIN) lesions in endogenous and reconstitution assays. Finally, both mouse and human RS are characterized by increases in TGF-M-NM-2 signaling heterogeneity immediately adjacent to PIN lesions; however, heterogeneity is lost during later stages of progression, likely contributing to tissue invasion. These studies confirm the importance of the FGFR1-Wnt-TGF-M-NM-2 signaling axes as driving forces behind reactive stroma and aggressive adenocarcinoma. To elucidate the mechanism behind the Wnt-accelerated FGFR1 adenocarcinoma, we performed laser capture microdissection (LCM) to separate pre-cancerous (hyperplasia and PIN) epithelia and adjacent reactive-stroma cells. We utilized frozen samples from specific time points (JOCK1, 40 weeks, Pro-Cat M-CM-^W JOCK1 and Ubi-Cat M-CM-^W JOCK1, 24 weeks) and performed gene expression profiling on the respective tissues.
2014-01-07 | E-GEOD-41344 | biostudies-arrayexpress
Project description:Transforming growth factor-β (TGF-β) is a key factor for the development of prostate cancer metastases in bone. In breast cancer and melanoma, studies have shown how TGF-β regulates gene expression to allow cancer cells to adapt to the bone microenvironment. We used microarray analyses to characterize the effect of TGF-β on gene expression in prostate cancer cells in vitro.
2014-11-01 | GSE58698 | GEO