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RNA-Immunoprecipitation of PIWIL1/piRNA complexes in COLO 205 cells and deep-sequencing of associated small RNAs with NGS technologies

ABSTRACT: RNA-Immunoprecipitation of PIWIL1/piRNA complexes in COLO 205 cells and deep-sequencing of associated small RNAs with NGS technologies

PROVIDER: PRJEB33352 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR3415730.fastq.gz	Fastqsanger.gz
	ERR3415740.fastq.gz	Fastqsanger.gz
	ERR3415731.fastq.gz	Fastqsanger.gz
	ERR3415732.fastq.gz	Fastqsanger.gz
	ERR3415733.fastq.gz	Fastqsanger.gz

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RNA-Immunoprecipitation of PIWIL1/piRNA complexes in COLO 205 cells and deep-sequencing of associated small RNAs with NGS technologies

Project description:To evaluate PIWIL1/piRNAs association in the metastatic COLO 205 cell line, we performed an RNA-immunoprecipitation experiment followed by small RNA deep-sequencing (RIP-Seq). For the identification of PIWIL1/piRNA complexes, independent reactions were carried out with two different antibodies (IP1 and IP2); non-specific interactions were computationally filtered out using a No Antibody control (No Ab).

2020-08-05 | E-MTAB-8121 | biostudies-arrayexpress

Transcriptome profiling of total RNA in the COLO 205 cell line with Next-Generation Sequencing (NGS) technologies

Project description:The transcriptome of COLO 205 cells was investigated using an RNA-Seq approach. This allowed us to evaluate the expression of mRNAs encoding for the major interactors of PIWIL proteins and factors involved in piRNAs biogenesis.

2020-08-06 | E-MTAB-8116 | biostudies-arrayexpress

Transcriptome profiling of total RNA in the COLO 205 cell line with Next-Generation Sequencing (NGS) technologies

Project description:Transcriptome profiling of total RNA in the COLO 205 cell line with Next-Generation Sequencing (NGS) technologies

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Analysis of the 3’-end of piRNAs in the COLO 205 cell line through sodium periodate (NaIO4) /β-Elimination treatment and small RNA-Seq

Project description:Using a chemical treatment, the sodium periodate (NaIO4) /β-Elimination oxidation, and then performing deep-sequencing of small RNAs with NGS technologies, we evaluated the methylation status of the piRNAs population in the metastatic COLO 205 cell line.

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Colo-205

Project description:Human Colo-205 (mitochondrial) cells

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Piwil1 Regulates Glioma Stem Cell Maintenance and Glioblastoma Progression

Project description:Piwi proteins are a subfamily of Argonaute proteins that maintain germ cells in eukaryotes. However, the role of their human homologues in cancer stem cells and more broadly in cancer is poorly understood. Here, we report that the Piwi-like family members, including Piwil1 (Hiwi), are overexpressed in glioblastoma (GBM), with Piwil1 levels most frequently elevated. Piwil1 is enriched in glioma stem cells (GSCs) and helps to maintain their self-renewal. GSCs were transduces with control non-targeting shRNAs (shNT) and shPiwil1 (#1 and #2) and global gene expression was analyzed to identify Piwil1 downscream singalings.

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piRNA-independent Function of PIWIL1 as a Novel co-activator for Anaphase Promoting Complex/Cyclosome (APC/C) to Drive Pancreatic Cancer Metastasis

Project description:Piwi proteins are normally restricted in germ cells to suppress transposons through association with piRNAs, but are also frequently activated in many types of human cancers. Of great puzzle is the lack of induction of corresponding piRNAs in cancer cells, as we document here in human pancreatic ductal adenocarcinomas (PDAC), implying that such germline-specific proteins are somehow hijacked to promote tumorigenesis through different mode of action. To pursue the underlying mechanism, we now demonstrate that in the absence of piRNAs, the aberrantly induced human PIWIL1 in PDAC functions as an oncoprotein by activating the Anaphase Promoting Complex/Cyclosome (APC/C), which then targets a critical cell adhesion-related protein Pinin to enhance PDAC metastasis. This is in contrast to piRNA-dependent PIWIL1 ubiquitination and removal by APC/C during late spermiogenesis. These findings thus unveil an piRNA-dependent mechanism to switch PIWIL1 from a substrate in spermatids to a co-activator of APC/C in human cancer cells.

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