Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1217928 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:PAX5 promotes progression of neuroendocrine prostate cancer
| PRJNA533095 | ENA
Project description:LSD1 promotes castration-resistant prostate cancer progression
| PRJNA311372 | ENA
Project description:Through digital rectal examinations and routine prostate-specific antigen (PSA) screening, early treatment of prostate cancer has become possible. However, prostate cancer is a complex and heterogeneous disease. In many patients, cancer cells can invade adjacent tissues and metastasize to other tissues, resulting in difficultly to cure. For the treatment of primary and metastatic prostate cancer, a significant problem is how to improve its survival time. Here, we collect 7 untreated primary and metastatic prostate cancer and 6 benign prostate hyperplasia samples under ultrasound guidance by experienced radiologists using the 18-G needle. Through mass spectrometry, we have completely depicted the protein atlas of primary and metastatic prostate cancer and benign prostate hyperplasia. Through bioinformatics analysis, experimental verification, and combined clinical data, we discover that the ribosome signaling pathway promotes the progression of prostate cancer and is associated with a poor prognosis. Among them, Mrpl1, Mrpl4, and Mrpl16 may be biomolecular markers for diagnosis and prognosis.
2021-09-05 | PXD028211 |
Project description:EphA6 promotes angiogenesis and prostate cancer metastasis and is associated with human prostate cancer progression
| PRJNA276564 | ENA
Project description:ERβ activation by genistein promotes metastatic progression in prostate cancer
| PRJNA184722 | ENA
Project description:The placental gene PEG10 promotes progression of neuroendocrine prostate cancer
| PRJEB9660 | ENA
Project description:The placental gene PEG10 promotes progression of neuroendocrine prostate cancer
| PRJNA257211 | ENA
Project description:The current view of cellular transformation and cancer progression supports the notion that cancer cells must reprogram their metabolism in order to survive and progress in different microenvironments. Master co-regulators of metabolism orchestrate the modulation of multiple metabolic pathways through transcriptional programs, and hence constitute a probabilistically parsimonious mechanism for general metabolic rewiring. Here we show that the transcriptional co-activator PGC1α suppresses prostate cancer progression and metastasis. A metabolic co-regulator data mining analysis unveiled that PGC1α is consistently down-regulated in multiple prostate cancer patient datasets and its alteration is associated with reduced disease-free survival and metastasis. Genetically engineered mouse model studies revealed that compound prostate epithelium-specific deletion of Pgc1a and Pten promotes prostate cancer progression and metastasis, whereas, conversely, PGC1α expression in cell lines inhibits the pre-existing metastatic capacity. Through the application of integrative metabolomics and transcriptomics we demonstrate that PGC1α expression in prostate cancer is sufficient to elicit a global metabolic rewiring that opposes cell growth, consisting of sustained oxidative metabolism at the expense of anabolism. This metabolic program is regulated downstream the Oestrogen-related receptor alpha (ERRα), and PGC1α mutants lacking ERRα activation capacity lack metabolic rewiring capacity and metastasissuppressive function. Importantly, an ERRα signature in prostate cancer recapitulates the prognostic features of PGC1A. Our findings uncover an unprecedented causal contribution of PGC1α to the metabolic switch in prostate cancer and to the suppression of metastatic dissemination. Total RNA was isolated from prostate cancer cell line PC3 expressing or not PGC1a (for induction, cells were treated with doxycycline for 2 passages)
2016-03-16 | E-GEOD-75193 | biostudies-arrayexpress
Project description:Prostate glands predominantly exhibit androgen dependence, but increasing evidence suggests that estrogen receptor signaling is involved in its development and pathogenesis. By integrating ChIP sequencing for estrogen receptor alpha (ERα) with transcriptome sequencing data from prostate cancer samples, we found ERα to significantly influence the noncoding transcriptome in prostate cancer. We identified one such long noncoding RNA, NEAT1, to play an important role in prostate cancer progression through direct regulation of transcription of its target genes. NEAT1, in an ERα dependent manner, promotes prostate tumorigenesis by interacting with and modulating chromatin state at promoters of prostate cancer specific signature genes. NEAT1 expression is positively correlated with PSMA in prostate adenocarcinoma and with B3GAT1 in neuroendocrine prostate cancer. This study identifies NEAT1 as a novel biomarker or therapeutic target in prostate cancer and also suggests that co-targeting ERα and androgen receptor (AR) may be effective for a subset of patients with advanced prostate cancer and with NEAT1 overexpression.
2014-12-01 | GSE43985 | GEO