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TSPAN18 facilitates bone metastasis of prostate cancer by protecting STIM1 from TRIM32-mediated ubiquitination

ABSTRACT: TSPAN18 facilitates bone metastasis of prostate cancer by protecting STIM1 from TRIM32-mediated ubiquitination

PROVIDER: PRJNA898409 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22197004_1.fastq.gz	Fastqsanger.gz
	SRR22197004_2.fastq.gz	Fastqsanger.gz
	SRR22197005_1.fastq.gz	Fastqsanger.gz
	SRR22197005_2.fastq.gz	Fastqsanger.gz
	SRR22197006_1.fastq.gz	Fastqsanger.gz

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TSPAN18 facilitates bone metastasis of prostate cancer by protecting STIM1 from TRIM32-mediated ubiquitination

Project description:We demonstrated that TSPAN18 was overexpressed in prostate cancer (PCa) and markedly accelerated PCa cell migration and invasion in vitro and bone metastasis in vivo by inhibiting E3 ligase tripartite motif containing 32 (TRIM32)-mediated stromal interaction molecule ubiquitination and degradation. To further investigate the genes regulated by TSPAN18, we knockdown TSPAN18 by siRNA and performed high-throughput sequence. So we identify a series of genes regulated by TSPAN18.

2023-01-01 | GSE217342 | GEO

TSPAN18 facilitates bone metastasis of prostate cancer by protecting STIM1 from TRIM32-mediated ubiquitination.

Project description:BackgroundBone metastasis is a principal cause of mortality in patients with prostate cancer (PCa). Increasing evidence indicates that high expression of stromal interaction molecule 1 (STIM1)-mediated store-operated calcium entry (SOCE) significantly activates the calcium (Ca2+) signaling pathway and is involved in multiple steps of bone metastasis in PCa. However, the regulatory mechanism and target therapy of STIM1 is poorly defined.MethodsLiquid chromatography-mass spectrometry analysis was performed to identify tetraspanin 18 (TSPAN18) as a binding protein of STIM1. Co-IP assay was carried out to explore the mechanism by which TSPAN18 inhibits STIM1 degradation. The biological function of TSPAN18 in bone metastasis of PCa was further investigated in vitro and in vivo models.ResultWe identified that STIM1 directly interacted with TSPAN18, and TSPAN18 competitively inhibited E3 ligase tripartite motif containing 32 (TRIM32)-mediated STIM1 ubiquitination and degradation, leading to increasing STIM1 protein stability. Furthermore, TSPAN18 significantly stimulated Ca2+ influx in an STIM1-dependent manner, and then markedly accelerated PCa cells migration and invasion in vitro and bone metastasis in vivo. Clinically, overexpression of TSPAN18 was positively associated with STIM1 protein expression, bone metastasis and poor prognosis in PCa.ConclusionTaken together, this work discovers a novel STIM1 regulative mechanism that TSPAN18 protects STIM1 from TRIM32-mediated ubiquitination, and enhances bone metastasis of PCa by activating the STIM1-Ca2+ signaling axis, suggesting that TSPAN18 may be an attractive therapeutic target for blocking bone metastasis in PCa.

| S-EPMC10403854 | biostudies-literature

HDAC2 facilitates metastasis of pancreatic cancer cells

Project description:HDAC2 facilitates pancreatic cancer metastasis

| PRJEB47385 | ENA

Expression profile of select glucose and lipid metabolic genes mediated by STIM1 knockout, or STIM1 knockout plus Snail1 overexpression in SMMC7721 cells

Project description:To investigate the altered glucose and lipid metabolism genes after STIM1 knockout (STIM1 KO) or STIM1 knockout plus Snail1 OE (STIM1 KO+Snail1 OE) in SMMC7721 cells. STIM1 KO-SMMC7721 cells were constructed by CRISPR/Cas9, and STIM1 KO+Snail1 OE-SMMC7721 cells was established via lentiviral Infection of Snail1 overexpression in STIM1 KO-SMMC7721 cells. The cells mentioned above were cultured in DMEM supplemented with 10% (v/v) FBS at 37 °C in 5% CO2. When the cells grow to 60~70% confluent, total RNA was extracted by using Trizol (TAKARA, Japan). Reverse transcription was performed from 1μg total RNA using PrimeScript™ RT reagent Kit with gDNA Eraser (TAKARA), Quantitative real-time PCR were performed (CFX386, BioRad) with 40 cycles at 95 °C for 10 seconds, 59 °C for 20 seconds and 72 °C for 30 seconds.

2020-04-07 | GSE148129 | GEO

STIM1 Translocation to The Nucleus Protects Cells from DNA Damage

Project description:DNA damage represents a challenge for cells as this damage must be eliminated to preserve cell viability and the transmission of genetic information. To reduce or eliminate unscheduled chemical modifications in genomic DNA, an extensive signaling network, known as the DNA damage response (DDR) pathway, ensures this repair. In this work, and by means of a proteomic analysis aimed at the study of the STIM1 protein interactome, we have found that STIM1 is closely related to the protection from endogenous DNA damage, replicative stress, as well as in the response to interstrand crosslinks (ICLs). Here we show that STIM1 has a nuclear localization signal (NLS) that mediates its translocation to the nucleus, and that this translocation and the association of STIM1 to chromatin is enhanced in response to mitomycin C (MMC), an ICL-inducing agent. Consequently, STIM1-deficient cell lines show a higher level of basal DNA damage, replicative stress, and a higher sensitivity to MMC. We show that STIM1 normalizes FANCD2 protein levels in the nucleus, explaining the increased sensitivity to MMC in STIM1-KO cells. Our results show for the first time a nuclear function for the endoplasmic reticulum protein STIM1 and increase the number of genes involved in DNA repair.

2023-12-22 | PXD041181 | Pride

Netrin-1 facilitates pancreatic cancer liver metastasis

Project description:Netrin-1 facilitates pancreatic cancer liver metastasis

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STIM1 controls T cell mediated immune regulation and inflammation in chronic infection

Project description:Influence of STIM1 on the transcriptome of CD4+ T cell subsets STIM1 is critical for the regulation of the intracellular Ca2+ homeostasis in CD4+ T cell. Loss of function mutations in STIM1 in patients result in severe immuno deficiency and recurrent infections. Using conditional knock out mice for STIM1, we investigated the role of STIM1 in T cells during chronic infections by in-vivo and in-vitro experiments. We found that STIM1 is required for T cell-mediated immunity to chronic infection with Mycobacterium tuberculosis (Mtb) as STIM1-deficient mice succumb to infection faster than littermate controls, have increased mycobacterial burdens and severe pulmonary infiltration with myeloid and lymphoid cells .Using the Affymetrix Mouse Exon 1.0 platform, we analyzed the influence of STIM1 expression on the transcriptom of CD4+T cells in-vitro. We found that STIM1 is required for the regulation of apoptosis related genes after TCR stimulation as well as for the induction of a transcriptonal program that polarizes naive CD4+ T cells into inducible CD4+ T regulatory cells (iTreg). Together with our in-vivo findings, these experiments reveal that STIM1 is essential for immune regulation to prevent an injurious inflammatory response during chronic infection.

2015-03-17 | GSE66933 | GEO

Transcriptome Stim1 R304W skeletal muscle

Project description:Comparative RNAseq of tibilias anterior from Stim1 R304W and WT male mice at 4 months

2021-07-07 | GSE179460 | GEO

Gene expression profile of STIM1 deficiency for cardiac remodeling in response to pressure overload by transverse aortic constriction (TAC)

Project description:STIM1 is a Ca2+ sensor of intracellular Ca2+ stores and essentially activates the Ca2+ entry channels of the plasma membrane. STIM1 is predicted to activate transient receptor potential canonical (TRPC) channels and Orai channels, and has a critical role in promoting the development of cardiac hypertrophy. Gene array experiments were performed to analyze the effects of STIM1 deficiency using total RNA from the left ventricles of WT sham, WT TAC, STIM1KO sham and STIM1KO TAC 4 weeks after the operation.

2014-07-01 | E-GEOD-38733 | biostudies-arrayexpress

STIM1-mediated gene expression in non-pathogenic and pathogenic CD4+ Th17 cells

Project description:Immunity to fungal infections is mediated by cells of the innate and adaptive immune system. Activation of immune cells requires Ca2+ influx through the Ca2+ channel ORAI1, which is activated by stromal interaction molecule 1 (STIM1). Th17 cells are essential for immunity to C. albicans infection and require Ca2+ influx for expression of IL-17A and other Th17 cytokines. In mice, deletion of STIM1 and thus Ca2+ influx in all immune cells enhanced susceptibility to mucosal C. albicans infection, whereas T cell-specific deletion of STIM1 impaired immunity to systemic C. albicans infection. STIM1 deletion in CD4 T cells had different effects on gene expression programs in pathogenic (proinflammatory) and non-pathogenic Th17 cells. STIM1 deletion in non-pathogenic Th17 cells, which are required for antifungal immunity, compromised the expression of genes in several metabolic pathways including Foxo and HIF-1a signaling as well as the TCA cycle and oxidative phosphorylation (OXPHOS). Consequently, STIM1 deficient non-pathogenic Th17 cells had impaired glycolysis and mitochondrial respiration. By contrast, STIM1 deletion in pathogenic Th17 cells showed only attenuated mitochondrial function but normal glycolysis.

2020-06-01 | GSE149162 | GEO

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