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SAM68 is a splicing regulator in triple negative breast cancer

ABSTRACT: SAM68 is a splicing regulator in triple negative breast cancer

PROVIDER: PRJNA590793 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10503186_1.fastq.gz	Fastqsanger.gz
	SRR10503186_2.fastq.gz	Fastqsanger.gz
	SRR10503187_1.fastq.gz	Fastqsanger.gz
	SRR10503187_2.fastq.gz	Fastqsanger.gz
	SRR10503188_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

SAM68 is a splicing regulator in triple negative breast cancer

Project description:SAM68 is an RNA binding protein frequently up-regulated in several human cancers and its oncogenic activity has often been associated with its splicing activity. Nevertheless, the genome-wide impact of SAM68 on the transcriptome of cancer cells is still unknown. Herein, by high-throughput RNA sequencing analysis of MDA-MB-231 SAM68-silenced cells, we uncover an extensive modulation of triple-negative breast cancer cell transcriptome by this splicing factor.

2022-04-04 | GSE140754 | GEO

SAM68 promotes Lung adenocarcinoma tumorigenesis by regulating cancer metabolic conversion through alternative splicing

Project description:The metabolic conversion of oxidative phosphorylation to glycolysis provides tumor cells with energy and biosynthetic substrates, thereby promoting tumorigenesis and malignant progression. However, the mechanisms controlling the tumor metabolic switch is still not entirely clear. Here we demonstrate that SAM68 (gene name: KHDRBS1) as a splicing regulatory factor is frequently overexpressed in Lung adenocarcinoma (LUAD) and negatively correlated with the prognosis of LUAD patients. we find SAM68 promotes LUAD cells tumorigenesis and metastasis both in vitro and in vivo by regulating cancer metabolic switch. SAM68 drives cancer metabolism by mediating alternative splicing of Pyruvate kinase (PKM) pre-mRNAs, finally promoting the formation of PKM2. Mechanically, Sam68 interacted with the splicing repressor hnRNP A1, and depletion of hnRNP A1 or mutations that impair this interaction attenuated the PKM splicing regulation. Together, our work demonstrates key roles of SAM68 in the cancer metabolic conversion by regulating alternative splicing and SAM68 may be a promising therapeutic target for treating LUAD.This project looks into how SAM68 levels affect cancer cell phenotype in vitro

2020-11-04 | GSE149120 | GEO

Sam68 regulation of alternative splicing in the developing cerebellum

Project description:We uncover a Sam68-dependent splicing program during cerebellar development. These events direct proper isoform expression of the genes required to guarantee the establishment of the correct spatial/temporal neural circuitry. The dysregulation in Sam68 null mice leads to functional defects in adult neurons

2020-06-01 | GSE133711 | GEO

SAM68-specific splicing is required for proper selection of alternative 3'UTR isoforms in the nervous system

Project description:Neuronal alternative splicing is dynamically regulated in a spatiotemporal fashion. We previously found that STAR family proteins (SAM68, SLM1, SLM2) regulate spatiotemporal alternative splicing in the nervous system. However, the whole aspect of alternative splicing programs governed by STARs remains unclear. We deciphered the alternative splicing programs of SAM68 and SLM1 proteins using transcriptomics. We reveal that SAM68 and SLM1 encode distinct alternative splicing programs; SAM68 preferentially controls alternative last exon (ALE) splicing. Interleukin 1-receptor accessory protein (Il1rap) is a novel target for SAM68. The usage of Il1rap ALEs results in mainly two variants encoding two functionally different isoforms, a membrane-bound (mIL1RAcP) and a soluble (sIL1RAcP) type. The brain exclusively expresses mIL1RAcP. SAM68 knockout results in remarkable conversion into sIL1RAcP in the brain, which significantly disturbs IL1RAcP neuronal function. Thus, we uncover the critical role of proper neuronal isoform selection through ALE choice by the SAM68-specific splicing program.

2019-12-29 | GSE110258 | GEO

Sam68 insures proper 3'-end pre-mRNA processing during germ cell differentiation

Project description:Male germ cells express the widest repertoire of transcript variants in mammalian tissues. Nevertheless, factors and mechanisms underlying such pronounced diversity are largely unknown. The splicing regulator Sam68 is highly expressed in meiotic cells and its ablation results in defective spermatogenesis. Herein, we uncover an extensive splicing program operated by Sam68 across meiosis, primarily characterized by alternative last exon (ALE) regulation in genes of functional relevance for spermatogenesis. Lack of Sam68 preferentially causes premature transcript termination at internal polyadenylation sites.

2019-03-12 | GSE122929 | GEO

Cdk1-mediated threonine phosphorylation of Sam68 modulates its RNA binding, alternative splicing activity, and cellular functions

Project description:Sam68 is a member of the STAR family of proteins that directly link signal transduction with post-transcriptional gene regulation. Sam68 controls the alternative splicing of many oncogenic proteins and its role is modulated by post-translational modifications, including serine/threonine phosphorylation, that differ at various stages of the cell cycle. However, the molecular basis and mechanisms of these modulations remain largely unknown. Here, we combined mass spectrometry, NMR spectroscopy, and cell biology techniques to provide a comprehensive post-translational modification (PTM) mapping of Sam68 at different stages of the cell cycle in HEK293 and HCT116 cells. We established that Sam68 is specifically phosphorylated at T33 and T317 by Cdk1, and demonstrated that these phosphorylation events reduce the binding of Sam68 to RNA, control its cellular localization, and reduce its alternative splicing activity, leading to a reduction in the induction of apoptosis and an increase in the proliferation of HCT116 cells.

2023-03-11 | PXD032716 | Pride

HMGA1: A master regulator of tumor progression in triple-negative breast cancer cells

Project description:Emerging evidence suggests that tumor cells metastasize by co-opting stem cell transcriptional networks, although the molecular underpinnings of this process are poorly understood. Here, we show for the first time that the high mobility group A1 (HMGA1) gene drives metastatic progression in triple negative breast cancer cells (MDA-MB-231) by reprogramming cancer cells to a stem-like state. We discovered an HMGA1 signature in triple negative breast cancer cells that is highly enriched in embryonic stem cells. Together, these findings indicate that HMGA1 is a master regulator of tumor progression in breast cancer by reprogramming cancer cells through stem cell transcriptional networks. Future studies are needed to determine how to target HMGA1 in therapy. HMGA1 was knocked-down in MDA-MB-231 cells using siRNA as we previously described (Tesfaye A 2007). RNA from three independent knockdown experiements along with 3 control populations were collected by Rneasy miniprep (Qiagen) and analyzed by Affymetrix Human Exon 1.0 ST platform.

2015-02-18 | E-GEOD-45483 | biostudies-arrayexpress

Sam68 regulation of alternative splicing in the developing cerebellum

Project description:Sam68 regulation of alternative splicing in the developing cerebellum

| PRJNA552299 | ENA

HMGA1: A master regulator of tumor progression in triple-negative breast cancer cells

2015-02-18 | GSE45483 | GEO

Splicing factors control triple-negative breast cancer cell mitosis through SUN2 interaction and sororin intron retention

Project description:Triple negative breast cancer (TNBC) is an aggressive subtype of breast cancer with limited therapeutic opportunities. Recently, splicing factors have gained attention as potential targets for cancer treatment. We performed an RNAi screen targeting 244 individual splicing factors to systematically evaluate their role in TNBC cell proliferation. We identified nine splicing factors, including SNRPD2, SNRPD3 and NHP2L1, of which depletion inhibited proliferation in two TNBC cell lines by deregulation of sister chromatid cohesion (SCC) via increased sororin intron 1 retention and down-regulation of SMC1, MAU2 and ESPL1. Protein-protein interaction analysis of SNRPD2, SNRPD3 and NHP2L1 identified that seven out of the nine identified splicing factors belong to the same spliceosome complex including novel componentSUN2 that was also critical for efficient sororin splicing. Finally, sororin transcript levels are highly correlated to various proliferation markers in BC patients, suggesting that deregulating sororin levels through targeting of the relevant splicing factors might be a potential strategy to treat TNBC

2021-03-07 | PXD013968 | Pride

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