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Exosomes mediate intercellular transference of non-autonomous tolerance to proteasome inhibitors in mixed-lineage leukemia.

ABSTRACT: Exosomes mediate intercellular transference of non-autonomous tolerance to proteasome inhibitors in mixed-lineage leukemia.

PROVIDER: PRJNA556681 | ENA |

REPOSITORIES: ENA

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Exosomes mediate intercellular transference of non-autonomous tolerance to proteasome inhibitors in mixed-lineage leukemia.

Project description:The interplay between cancer cells and microenvironment can influence treatment response and plays a key role in the emergence of drug resistance. Rapidly acquired resistance prevents proteasome inhibitors (PIs) therapies from achieving stable and complete responses. Investigating the underlying mechanisms and developing effective strategies against PI resistance are highly desired in the clinic. Here we uncovered that PI resistance was reversible in mixed-lineage leukemia (MLL), which consistent with the finding that patients could regain sensitivity to PIs after a drug holiday. Exosomes released from PI-treated cells could transmit PI resistance to sensitive cells via facilitating cell cycle arrest and stemness pathway in MLL cells. Furthermore, TieDIE algorithm integration analysis of transcriptome and proteome datasets identified candidate exosomal proteins, providing potential therapeutic targets for treating refractory MLL.

2020-04-22 | GSE134879 | GEO

Exosomes mediate intercellular transfer of non-autonomous tolerance to proteasome inhibitors in mixed-lineage leukemia.

Project description: Not available

| S-EPMC7156829 | biostudies-literature

Exosomes Mediate Intercellular Transmission of Porcine Reproductive and Respiratory Syndrome Virus.

Project description: Not available

| S-EPMC5790938 | biostudies-literature

Plasma membrane-derived extracellular microvesicles mediate non-canonical intercellular NOTCH signaling

Project description:ARMMs (arrestin domain-containing protein 1 [ARRDC1]-mediated microvesicles) are extracellular vesicles that bud directly atthe plasma membrane. However, little is known about the physiological function of these vesicles. Here we report that secreted ARMMs contain active NOTCH receptors and mediate a non-canonical intercellular NOTCH signaling. Masss pectrometry of purified ARMMs identifiedNOTCH2 as a protein component of the vesicles. The NOTCH protein in ARMMs contains the critical intracellular region (NICD) that is required for its transcriptional activity in the nucleus. ARRDC1 overexpression increased the NOTCH2 incorporation into ARMMs. Conversely, CRISPR-mediated knockout of ARRDC1 dramatically reduced the amount of NOTCH2 in secreted ARMMs. The incorporation of NOTCH2 into ARMMs is facilitated by the ITCH E3 ligase and ADAM10, which are also secreted into ARMMs. We showed NOTCH2 in ARMMs delivered into recipient cells is further activated by γ-secretase cleavage to induce NOTCH-specific signaling in recipient cells. Together, our findings revealed a role for ARMMs in a novelNOTCH signaling pathway that acts in distance beyond direct cell-cell contact.

2017-10-11 | PXD006416 | Pride

The proteasome subunit psmb1 is essential for craniofacial cartilage maturation and morphogenesis

Project description:Craniofacial dysmorphisms are among the most common birth defects. Proteasome mutations frequently result in craniofacial dysmorphisms including lower jaw malformations; however, the underlying mechanisms are unknown. Here we use a zebrafish proteasome subunit beta 1 (psmb1) mutant to define the cellular mechanisms underlying proteasome mutation-induced craniofacial dysmorphisms. psmb1 mutants exhibit a flattened ceratohyal and smaller Meckel’s and palatoquadrate cartilages. Ceratohyal flattening is a result of failed chondrocyte convergent extension, accompanied by reduced numbers of chondrocytes in the lower jaw due to defects in chondrocyte differentiation. Morphogenesis of craniofacial muscles and tendons is similarly perturbed. psmb1 mutants lack the hyohyal muscles and craniofacial tendons are shortened and disorganized. We additionally identify a critical period for proteasome function in craniofacial development, specifically during chondrocyte and muscle differentiation. psmb1 overexpression in sox10+ cells of mutant embryos rescued both cartilage and tendon phenotypes but induced only a partial rescue of the muscle phenotype, indicating that psmb1 is required in both tissue-autonomous and non-autonomous fashions during craniofacial development. Overall, our work demonstrates that psmb1 is required for craniofacial cartilage, tendon, and muscle differentiation and morphogenesis.

2024-07-12 | GSE243072 | GEO

Transcriptional profiling of Ewing's sarcoma derived exosomes

Project description:Exosomes are small RNA and protein containing vesicles that can mediate hetero- and homotypic intercellular communication between normal and malignant cells. Especially, tumor-derived exosomes are believed to mediate reprogramming of the tumor-associated stroma to favor tumor growth and metastasis. In this study we isolated exosomes from three different Ewing’s sarcoma (ES) cell lines by ultracentrifugation. Microarray analysis of ES-derived exosomes and their parental cells was performed to gain insight into the spectrum of transcripts they contain and the functions in which these transcripts might be involved in. In total we analyzed six different samples consisting of three pairs of exosomal and cellular RNA of different Ewing's sarcoma cell lines.

2013-05-01 | E-GEOD-42282 | biostudies-arrayexpress

MicroRNAs Mediate Insecticide Tolerance in Spodoptera frugiperda

Project description:MicroRNAs Mediate Insecticide Tolerance in Spodoptera frugiperda

| PRJNA785443 | ENA

Small extracellular vesicles are key regulators of non-cell autonomous intercellular communication in senescence via the interferon protein, IFITM3

Project description:Small extracellular vesicles are key regulators of non-cell autonomous intercellular communication in senescence via the interferon protein, IFITM3

| PRJNA543855 | ENA

PSMG2-controlled proteasome-autophagy balance mediates the tolerance for MEK targeted therapy in TNBC

Project description:We performed an unbiased genome-wide CRISPR/Cas9 knockout screening to identify synergistic drug targets in TNBC cells with MEK inhibitor. PSMG2 was found as a critical synthetically lethal gene with MEK inhibition. Mechanism investigation unraveled that PSMG2 knockdown inhibited proteasome function, which in turn activated cell autophagy. Autophagy, unlike its function in chemoresistance, inhibited PI3K/AKT pathway by specific degradation of PDPK1. Co-targeting MAPK pathway and proteasome pathway synergistically suppressed TNBC cells proliferation in vitro and in vivo.

2022-06-28 | GSE206748 | GEO

Transcriptional profiling of Ewing's sarcoma derived exosomes

2013-05-01 | GSE42282 | GEO

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