RNF185 control of COL3A1 expression impacts prostate cancer migration and metastatic potential
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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.
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