RNF185 control of COL3A1 expression impacts prostate cancer migration and metastatic potential
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA952534 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24078300.fastq.gz | Fastqsanger.gz | |||
| SRR24078301.fastq.gz | Fastqsanger.gz | |||
| SRR24078302.fastq.gz | Fastqsanger.gz | |||
| SRR24078303.fastq.gz | Fastqsanger.gz | |||
| SRR24078304.fastq.gz | Fastqsanger.gz |
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Project description:RNF185 is a RING finger domain-containing ubiquitin ligase implicated in ER associated degradation. Analysis of prostate tumor patient data revealed a negative correlation between RNF185 expression and prostate cancer progression and metastasis. Likewise, several prostate cancer cell lines exhibited greater migration and invasion capabilities in culture, upon RNF185 depletion. Subcutaneous inoculation of mouse prostate cancer MPC3 cells that stably express shRNA against RNF185 into B6 mice, resulted in larger tumors and more frequent lung metastases. RNA-sequencing and Ingenuity Pathway Analysis identified wound healing and cellular movement among the most significantly upregulated pathways in RNF185-depleted prostate cancer cells, compared with control. Gene Set Enrichment Analyses that were performed in both patients harboring low RNF185 expression, and in RNF185-depleted cell lines, confirmed deregulation of genes implicated in EMT. Among those, COL3A1 was identified as the primary mediator of RNF185 ability to impact the migration phenotype. Correspondingly, enhanced migration of RNF185 KD prostate cancer cells was abolished upon COL3A1 inhibition. Taken together, our results identify RNF185 as gatekeeper of prostate cancer metastasis, in part by its control of COL3A1 transcription.
2024-02-14 | GSE228999 | GEO
Project description:RNF185 is a RING finger domain-containing ubiquitin ligase implicated in ER-associated degradation. Prostate tumor patient data analysis revealed a negative correlation between RNF185 expression and prostate cancer progression and metastasis. Likewise, several prostate cancer cell lines exhibited greater migration and invasion capabilities in culture upon RNF185 depletion. Subcutaneous inoculation of mouse prostate cancer MPC3 cells stably expressing shRNA against RNF185 into mice resulted in larger tumors and more frequent lung metastases.RNA-sequencing and Ingenuity Pathway Analysis identified wound healing and cellular movement among the most significant pathways upregulated in RNF185-depleted, compared to control prostate cancer cells. Gene Set Enrichment Analyses performed in samples from patients harboring low RNF185 expression and in RNF185-depleted lines confirmed the deregulation of genes implicated in EMT. Among those, COL3A1 was identified as the primary mediator of RNF185’s ability to impact migration phenotypes. Correspondingly, enhanced migration and metastasis of RNF185 KD prostate cancer cells were attenuated upon co-inhibition of COL3A1. Our results identify RNF185 as a gatekeeper of prostate cancer metastasis, partly via its control of COL3A1 availability.
2024-08-09 | PXD045473 | Pride
Project description:RNF185 is a RING finger domain-containing ubiquitin ligase implicated in ER-associated degradation. Prostate tumor patient data analysis revealed a negative correlation between RNF185 expression and prostate cancer progression and metastasis. Likewise, several prostate cancer cell lines exhibited greater migration and invasion capabilities in culture upon RNF185 depletion. Subcutaneous inoculation of mouse prostate cancer MPC3 cells stably expressing shRNA against RNF185 into mice resulted in larger tumors and more frequent lung metastases. RNA-sequencing and Ingenuity Pathway Analysis identified wound healing and cellular movement among the most significant pathways upregulated in RNF185-depleted, compared to control prostate cancer cells. Gene Set Enrichment Analyses performed in samples from patients harboring low RNF185 expression and in RNF185- depleted lines confirmed the deregulation of genes implicated in EMT. Among those, COL3A1 was identified as the primary mediator of RNF185's ability to impact migration phenotypes. Correspondingly, enhanced migration and metastasis of RNF185 KD prostate cancer cells were attenuated upon coinhibition of COL3A1. Our results identify RNF185 as a gatekeeper of prostate cancer metastasis, partly via its control of COL3A1 availability.
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Project description:To identify genes with the potential target of differentially expressed miRNA in metastatic prostate cancer, we have employed whole genome microarray expression profiling. Transplantable metastatic versus a non-metastatic prostate cancer xenograft line, both derived from one patient’s primary cancer, were developed via sub-renal capsule grafting of cancer tissue into NOD/SCID mice. The same RNA samples from both lines were also used for miRNA sequencing. Overlapped genes of predicted targets of differentially expressed miRNAs and differentially expressed in microarray platform showed potential markers of combination of miRNA and gene in metastatic prostate cancer. Gene expression in metastatic/non-metastatic prostate cancer was measured. Same total RNA samples were used for small RNA library construction for miRNA sequencing. This submission represents the gene expression component of the study.
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Project description:Metastatic prostate cancer (PCa) is a terminal disease and establishment of novel therapeutic strategy specifically targeting metastasis is critically required for its management. This study was aimed at identifying metastasis-driving genes which could potentially be therapeutic targets for metastatic prostate cancer. Integrative analysis of gene expression profiles from a pair of metastatic and non-metastatic prostate cancer tissue xenografts was used to identify potential prostate cancer metastasis-driving genes. Among the candidate genes found, GATA2, a master regulator gene in the development of hematopoietic system, was particularly interesting since it is an important pioneer factor in the regulation of AR-target gene in prostate cancer. In consistent with our finding, elevated expression of the GATA2 gene in metastatic prostate cancers was found and its expression was significantly correlated with poor prognosis in prostate cancer patients. Furthermore, indication of the GATA2 gene maybe the metastasis-driving gene was evidenced in decreased of cell migration, tissue invasion and focal adhesion disassembly in GATA2-down-regulated LNCaP cells. Global gene expression analysis after silencing of the GATA2 gene revealed a significant changed in cell transcriptomes with ~ 2500 genes with > 2 fold mRNA level changed and FDR <0.05, indicates that GATA2 plays a critical role in cell reprogramming as pioneer factor in the development of prostate cancer metastasis. LNCaP human prostate cancer cells transiently knockdown with siRNA that specifically targeting GATA2 (siGATA2) or scrambled siRNA (sicontrol). RNAs were isolated from cells after 72 hours of incubation. Gene expression profiles of four biological replicates from each sample group were analyzed to identify differentially regulated downstream genes after knockdown of GATA2.
2014-01-20 | E-GEOD-49342 | biostudies-arrayexpress
Project description:To identify genes with the potential target of differentially expressed miRNA in metastatic prostate cancer, we have employed whole genome microarray expression profiling. Transplantable metastatic versus a non-metastatic prostate cancer xenograft line, both derived from one patient’s primary cancer, were developed via sub-renal capsule grafting of cancer tissue into NOD/SCID mice. The same RNA samples from both lines were also used for miRNA sequencing. Overlapped genes of predicted targets of differentially expressed miRNAs and differentially expressed in microarray platform showed potential markers of combination of miRNA and gene in metastatic prostate cancer.
2012-03-11 | GSE28029 | GEO
Project description:Metastatic prostate cancer (PCa) is a terminal disease and establishment of novel therapeutic strategy specifically targeting metastasis is critically required for its management. This study was aimed at identifying metastasis-driving genes which could potentially be therapeutic targets for metastatic prostate cancer. Integrative analysis of gene expression profiles from a pair of metastatic and non-metastatic prostate cancer tissue xenografts was used to identify potential prostate cancer metastasis-driving genes. Among the candidate genes found, GATA2, a master regulator gene in the development of hematopoietic system, was particularly interesting since it is an important pioneer factor in the regulation of AR-target gene in prostate cancer. In consistent with our finding, elevated expression of the GATA2 gene in metastatic prostate cancers was found and its expression was significantly correlated with poor prognosis in prostate cancer patients. Furthermore, indication of the GATA2 gene maybe the metastasis-driving gene was evidenced in decreased of cell migration, tissue invasion and focal adhesion disassembly in GATA2-down-regulated LNCaP cells. Global gene expression analysis after silencing of the GATA2 gene revealed a significant changed in cell transcriptomes with ~ 2500 genes with > 2 fold mRNA level changed and FDR <0.05, indicates that GATA2 plays a critical role in cell reprogramming as pioneer factor in the development of prostate cancer metastasis.
2014-01-20 | GSE49342 | GEO
Project description:Prostate cancer is characterized by heterogeneity in the clinical course that often does not to correlate with morphologic features of the tumor. Metastasis reflects the most adverse outcome of prostate cancer, and to date there are no reliable morphologic features or serum biomarkers that can reliably predict which patients are at higher risk of developing metastatic disease. Understanding the differences in the biology of metastatic and organ confined primary tumors is essential for developing new prognostic markers and therapeutic targets. Using Affymetrix oligonucleotide arrays, we analyzed gene expression profiles of 24 androgen-ablation resistant metastatic samples obtained from 4 patients and a previously published dataset of 64 primary prostate tumor samples. Differential gene expression was analyzed after removing potentially uninformative stromal genes, addressing the differences in cellular content between primary and metastatic tumors. The metastatic samples are highly heterogeneous in expression; however, differential expression analysis shows that 415 genes are upregulated and 364 genes are downregulated at least 2 fold in every patient with metastasis. The expression profile of metastatic samples reveals changes in expression of a unique set of genes representing both the androgen ablation related pathways and other metastasis related gene networks such as cell adhesion, bone remodeling and cell cycle. The differentially expressed genes include metabolic enzymes, transcription factors such as Forkhead Box M1 (FoxM1) and cell adhesion molecules such as Osteopontin (SPP1). We hypothesize that these genes have a role in the biology of metastatic disease and that they represent potential therapeutic targets for prostate cancer. Experiment Overall Design: Using Affymetrix oligonucleotide arrays, we analyzed gene expression profiles of 24 androgen-ablation resistant metastatic samples obtained from 4 patients and a previously published dataset of 64 primary prostate tumor samples. Differential gene expression was analyzed after removing potentially uninformative stromal genes, addressing the differences in cellular content between primary and metastatic tumors.
2008-06-15 | E-GEOD-6605 | biostudies-arrayexpress
Project description:An integrative analysis of this compendium of proteomic alterations and transcriptomic data was performed revealing only 48-64% concordance between protein and transcript levels. Importantly, differential proteomic alterations between metastatic and clinically localized prostate cancer that mapped concordantly to gene transcripts served as predictors of clinical outcome in prostate cancer as well as other solid tumors. Keywords: prostate cancer progression 13 individual benign prostate, primary and metastatic prostate cancer samples and 6 pooled samples from benign,primary or metastatic prostate cancer tissues.
2005-09-20 | E-GEOD-3325 | biostudies-arrayexpress
Project description:Purpose: Prostate cancer is the most frequently diagnosed cancer in men and the third leading cause of cancer related deaths among men living in developed countries. Biomarkers that predict disease outcome at the time of initial diagnosis would aid management of the disease. Experimental design: Proteins extracted from formalin-fixed paraffin-embeddded sections were identified either using LC-MALDI MS/MS of tryptic digests or after separation by one- or two-dimensional electrophoresis. A list of potential biomarker candidates, based on proposed associations with prostate cancer, was derived from the 320 identified proteins. Results: Four of the candidates: annexin A2, peroxiredoxin-1, prostate-specific antigen and zinc-alpha-2-glycoprotein, were examined by Western blotting of extracts of biopsies from men whom there was 10-year disease outcome data. Multiplexed Western blotting using cocktails of antibodies and fluor-labeled detection reagents showed that annexin A2 provided the best prediction of risk of metastatic disease. Conclusions and clinical relevance: This pilot study indicates that tumour expression of ANXA2 in diagnostic biopsies of a prostate cancer is predictive for the metastatic potential of that cancer. The potential of protein profiling of each cancer is to lead to an overall reduction in mortality from metastatic prostate cancer as well as reduced treatment associated morbidity.
2015-09-14 | PXD000963 | Pride