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PSAT1 drives extracellular vesicle release in multiple types of cancer and promotes bone metastasis by activating osteoclasts

ABSTRACT: PSAT1 drives extracellular vesicle release in multiple types of cancer and promotes bone metastasis by activating osteoclasts

PROVIDER: PRJNA768649 | ENA |

REPOSITORIES: ENA

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PSAT1 drives extracellular vesicle release in multiple types of cancer and promotes bone metastasis by activating osteoclasts

Project description:Cancer cells secrete extracellular vesicles (EVs) to regulate cells in the tumor microenvironment for their own benefit to grow and survive in the patient’s body. Although emerging evidence has demonstrated the molecular mechanisms of EV release, regulating cancer-specific EV secretion remains challenging . In this study, we applied a microRNA (miRNA) library to reveal the universal mechanisms of EV secretion in cancer cells. Here, we identified miR-891b and its direct target gene, phospho-aminotransferase 1 (PSAT1), which promotes EV secretion through the serine-ceramide synthesis pathway. Inhibition of PSAT1 affected EV secretion in multiple types of cancer, suggesting that the miR-891b/PSAT1 axis shares a common mechanism of cancer EV secretion.

2021-10-07 | GSE185312 | GEO

Directional endothelial communication by polarized extracellular vesicle release

Project description:Directional endothelial communication by polarized extracellular vesicle release

| PRJNA958118 | ENA

Directional endothelial communication by polarized extracellular vesicle release

Project description:Directional endothelial communication by polarized extracellular vesicle release

| PRJNA967339 | ENA

Directional endothelial communication by polarized extracellular vesicle release

Project description:Directional endothelial communication by polarized extracellular vesicle release

| PRJNA958200 | ENA

Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts

Project description:The hormone calcitonin (CT) is primarily known for its pharmacologic action as an inhibitor of bone resorption, yet CT-deficient mice display increased bone formation. These findings raised the question about the underlying cellular and molecular mechanism of CT action. Here we show that either ubiquitous or osteoclast-specific inactivation of the murine CT receptor (CTR) causes increased bone formation. CT negatively regulates the osteoclast expression of Spns2 gene, which encodes a transporter for the signaling lipid sphingosine 1-phosphate (S1P). CTR-deficient mice show increased S1P levels, and their skeletal phenotype is normalized by deletion of the S1P receptor S1P3. Finally, pharmacologic treatment with the non-selective S1P receptor agonist FTY720 causes increased bone formation in wildtype, but not in S1P3-deficient mice. This study redefines the role of CT in skeletal biology, confirms that S1P acts as an osteoanabolic molecule in vivo, and provides evidence for a pharmacologically exploitable crosstalk between osteoclasts and osteoblasts. Osteoclasts of wildtype and Calcr-/- C57Bl/6 mice were treated with Calcitonin and compared to the non-treated osteoclasts of wildtype or Calcr-/- mice, respectively.

2014-10-19 | E-GEOD-60761 | biostudies-arrayexpress

Dynamin-like proteins are essential for vesicle biogenesis in Mycobacterium tuberculosis.

Project description:Mycobacterium tuberculosis (Mtb) secretes pathogenicity factors and immunologically active molecules via membrane vesicles. However, nothing is known about the mechanisms involved in mycobacterial vesicle biogenesis. This study investigates molecular determinants of membrane vesicle production in Mtb by analyzing Mtb cells under conditions of high vesicle production: iron limitation and VirR restriction. Ultrastructural analysis showed extensive cell envelope restructuring in association with vesicle release that correlated with downregulation of cell surface lipid biosynthesis and peptidoglycan alterations. Comparative transcriptomics showed common upregulation of the iniBAC operon in association with high vesicle production in Mtb cells. Vesicle production analysis demonstrated that the dynamin-like proteins (DLPs) encoded by this operon, IniA and IniC, are necessary for release of EV by Mtb in culture and in infected macrophages. Isoniazid, a first-line antibiotic, used in tuberculosis treatment, was found to stimulate vesicle release in a DLP-dependent manner. Our results provide a new understanding of the function of mycobacterial DLPs and mechanistic insights into vesicle biogenesis. The findings will enable further understanding of the relevance of Mtb-derived extracellular vesicles in the pathogenesis of tuberculosis and may open new avenues for therapeutic research.

2023-06-22 | GSE143996 | GEO

Analysis of a long noncoding RNAs that modulate neurotransmitter release

Project description:We report the application of a novel integrated screening strategy to identify lncRNAs that regulate synaptic vesicle release. We identified one of these lncRNAs, which is conserved across mammals, neuron-specific and strictly nuclear. Modulations of this lncRNA influence synaptic vesicle release, presynaptic calcium influx, neurite elongation and neuronal migration. We have characterized the DNA, RNA and protein inteactors of this lncRNA and clarified its involvement in the stabilization of mRNAs for synaptic vesicle proteins.

2020-04-10 | GSE131103 | GEO

Murine Osteoclasts: Stat5 flox vs. Stat5 cKO

Project description:Transcriptional profiling of mouse osteoclasts comparing control osteoclasts from Stat5 flox mice with osteoclasts from Stat5 cKO mice. Two-condition experiment, Stat5 flox cells vs. Stat5 cKO cells

2013-12-09 | E-GEOD-51283 | biostudies-arrayexpress

Murine Osteoclasts: Stat5 flox vs. Stat5 cKO

Project description:Transcriptional profiling of mouse osteoclasts comparing control osteoclasts from Stat5 flox mice with osteoclasts from Stat5 cKO mice.

2013-12-09 | GSE51283 | GEO

Expression profile of osteoclasts treated with bisphosphonates

Project description:Bisphosphonates are the mainstay of therapy worldwide for osteoporosis. They inhibit the activities of the osteoclasts, the bone resorption cells. While bisphosphonates are known to block farnesyl pyrophsophate synthase to exert their anti-resorptive action, the detailed mechanism is not well understood. Examining the change in expression profile before and after bisphosphonate treatment in the osteoclasts might shed some light on the biological pathways that are perturbed. Osteoclastic precursor cells were treated with (or without) bisphosphonates (alendronate or risedronate) during their differentiation into mature osteoclasts.

2014-11-06 | E-GEOD-63009 | biostudies-arrayexpress

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