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Homo sapiens

ABSTRACT: The epigenetic reader protein SPIN1 controls proliferation and survival of liposarcoma by modulating the RET signaling pathway [ChIP-Seq]

PROVIDER: PRJNA246554 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR1282273.fastq.gz	Fastqsanger.gz
	SRR1282274.fastq.gz	Fastqsanger.gz
	SRR1282275.fastq.gz	Fastqsanger.gz
	SRR1282276.fastq.gz	Fastqsanger.gz
	SRR1569513.fastq.gz	Fastqsanger.gz

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The epigenetic reader protein SPIN1 controls proliferation and survival of liposarcoma by modulating the RET signaling pathway

Project description:The epigenetic reader protein SPIN1 controls proliferation and survival of liposarcoma by modulating the RET signaling pathway

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Homo sapiens

Project description:The epigenetic reader protein SPIN1 controls proliferation and survival of liposarcoma by modulating the RET signaling pathway [RNA-Seq]

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The epigenetic reader protein SPIN1 controls proliferation and survival of liposarcoma by modulating the RET signaling pathway [RNA-Seq]

Project description:The aim of this study is to identify the SPIN1 target genes in liposarcoma cells

2017-02-09 | GSE57501 | GEO

The epigenetic reader protein SPIN1 controls proliferation and survival of liposarcoma by modulating the RET signaling pathway [ChIP-Seq]

Project description:The aim of this study is to identify the SPIN1 target genes in liposarcoma cells

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Project description:The histone code reader Spin1 controls skeletal muscle development

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SPIN1 accelerates tumorigenesis and confers radioresistance of non-small cell lung cancer via orchestrating the FOXO3a/FOXM1 axis

Project description:Radioresistance is a predominant obstacle of effective treatments in non-small cell lung cancer (NSCLC), while the underlying mechanism remains incompletely elucidated. Spindlin 1(SPIN1) has been reported to participate in tumor initiation and progression, while its role in NSCLC tumorigenesis and radioresistance remains largely unknown. In this study, bioinformatics analysis, immunohistochemistry (IHC) and western blotting assays were performed to test SPIN1 expression in NSCLC samples and cell lines. The carcinogenic role of SPIN1 was evaluated by cell growth and proliferation, EdU staining, transwell and colony formation assays. Besides, the radiosensitivity of NSCLC cells was determined by clonogenic cell survival, neutral comet and γ-H2AX and Rad51 foci formation assays. Xenograft tumor model was constructed to access the effects of SPIN1 on tumorigenesis and radiosensitivity. Furthermore, RNA sequencing, quantitative real-time PCR, CHX and ubiquitination assays were applied to elucidate the correlation between SPIN1 and FOXO3a-FOXM1 axis. Therefore, our results suggest that the SPIN1-MDM2-FOXO3a/FOXM1 signaling axis is essential for NSCLC progression and radioresistance, and it could serve as therapeutic targets in irradiation-resistance NSCLC.

2024-11-20 | GSE276500 | GEO

Two-factor authentication underpins the precision of piRNA-directed LINE1 DNA methylatio

Project description:The PIWI-interacting RNA (piRNA) pathway guides the DNA methylation of young active transposons during male mouse germline development. piRNAs tether the PIWI protein MIWI2 (PIWIL4) to the nascent transposon transcript that results in DNA methylation through SPOCD1. Transposon methylation requires exacting precision: all copies need to be methylated yet, at the same time, off-target methylation must be avoided. However, the underlying mechanisms that ensure this precision remain unknown. Here, we show that SPOCD1 directly interacts with SPIN1 (SPINDLIN1), a chromatin reader that primarily binds H3K4me3 K9me3. The prevailing assumption is that all molecular events required for piRNA-directed DNA methylation occur after the engagement of MIWI2. Interestingly, we find that SPIN1 expression precedes that of both SPOCD1 and MIWI2. Furthermore, we demonstrate that young LINE1s, but not old copies are marked by H3K4me3, H3K9me3 and SPIN1 prior to the initiation of piRNA-directed DNA methylation. We generated a Spocd1 separation-of-function allele in the mouse that encodes a SPOCD1 variant that no longer interacts with SPIN1. We found that the SPOCD1-SPIN1 interaction is essential for spermatogenesis and piRNA-directed DNA methylation of young LINE1 elements. We propose that young LINE1 elements require a two-factor authentication process for DNA methylation, the first being the recruitment of SPIN1-SPOCD1 to licence the locus and the second is MIWI2 engagement with the nascent transcript, which is also the trigger for methylation. In summary, independent events that licence, and trigger methylation underpin the basis of precision.

2024-07-23 | GSE269344 | GEO

Two-factor authentication underpins the precision of piRNA-directed LINE1 DNA methylation

Project description:The PIWI-interacting RNA (piRNA) pathway guides the DNA methylation of young active transposons during male mouse germline development. piRNAs tether the PIWI protein MIWI2 (PIWIL4) to the nascent transposon transcript that results in DNA methylation through SPOCD1. Transposon methylation requires exacting precision: all copies need to be methylated yet, at the same time, off-target methylation must be avoided. However, the underlying mechanisms that ensure this precision remain unknown. Here, we show that SPOCD1 directly interacts with SPIN1, a chromatin reader that primarily binds H3K4me3 and this association is augmented by H3K9me3. The prevailing assumption is that all molecular events required for piRNA-directed DNA methylation occur after the engagement of MIWI2. Interestingly, we find that SPIN1 expression precedes that of both SPOCD1 and MIWI2. Furthermore, we demonstrate that young LINE1s, but not old copies are marked by H3K4me3 and H3K9me3 prior to the initiation of piRNA-directed DNA methylation. We generated a Spocd1 separation-of-function allele in the mouse that encodes a SPOCD1 variant that no longer interacts with SPIN1. We found that the SPOCD1-SPIN1 interaction is essential for spermatogenesis and piRNA-directed DNA methylation of young LINE1 elements. We propose that young LINE1 elements require a two-factor authentication process for DNA methylation, the first being the recruitment of SPIN1-SPOCD1 to licence the locus and the second is MIWI2 engagement with the nascent transcript, which is the trigger for methylation. In summary, independent events that licence, and trigger methylation underpin the basis of precision.

2024-09-04 | PXD041214 | Pride

Gene expression profiling of myxoid liposarcomas (validation set INT-B)

Project description:FUS-CHOP and EWS-CHOP balanced translocations characterize myxoid liposarcoma which encompasses myxoid (ML) and round cell (RC) variants initially believed to be distinct diseases. Currently, myxoid and RC liposarcoma are regarded to represent the well differentiated and the poorly differentiated ends, respectively, within spectrum of myxoid liposarcoma where the fusion proteins blocking lipogenic differentiation play a role in tumor initiation while molecular determinants associated to progression to RC remain poorly understood. Activation of AKT pathway sustained by PIK3CA and PTEN mutations and growth factor receptor signalling such as RET and IGF1R have been recently correlated with the increasing of aggressiveness and RC. Aim of the present study is to elucidate molecular events involved in driving round cell progression analyzing two small series of MLS selected to be representative of the two end of the gamut: the pure myxoid (0% of RC component) and RC with high cellular component (≥80%).

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Gene expression profiling of myxoid liposarcomas (training set INT-A)

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