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Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
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After budding out from the ER membrane, some COPII vesicles lose their coat and fuse with one another to form larger vesicles and interconnected tubules called vesicular tubular clusters or VTCs. These clusters constitute a compartment at the ER-Golgi interface known as ERGIC (Endoplasmic Reticulum Golgi Intermediate Compartment). The ERGIC is a mobile membrane-bound cargo transport system that sorts proteins secreted from ER and delivers them to the Golgi.
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Secretory vesicles, also known as dense core vesicles (DCVs), are membrane-bound vesicles that transport secretory proteins, such as hormones or neurotransmitters. Regulated secretory vesicles transport proteins from the trans-Golgi network to the exterior of the cell. Proteins present in regulated secretory vesicles are required to be rapidly exocytosed in large amounts upon a specific stimulus.
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Clathrin-coated vesicles use endocytosis to transport receptors and lysosomal hydrolases from the Golgi to the lysosome in the late secretory pathway. Clathrin-mediated endocytosis was the first described endocytic process, and Clathrin-coated vesicles remain one of the most well-studied transport vesicles. The molecular machinery that generates clathrin-coated vesicles comprises over 50 proteins that precisely coordinate vesicle formation. Cell surface receptors concentrated in indented sites...
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Microbial communities are dynamic environments where cell lysis releases free DNA into the surroundings. Other cells can take up this extracellular DNA through a process known as transformation.When a cell incorporates this foreign DNA into its genome, resulting in genetic modification, the process is known as transformation. Cells capable of this process are termed competent. Competence can be natural, as observed in certain bacteria and archaea, or artificially induced in the...
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In Vivo Immunogenicity Screening of Tumor-Derived Extracellular Vesicles by Flow Cytometry of Splenic T Cells
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Microvesicle Cargo and Function Changes upon Induction of Cellular Transformation.

Bridget T Kreger1, Andrew L Dougherty1, Kai Su Greene1

  • 1From the Departments of Molecular Medicine and.

The Journal of Biological Chemistry
|July 22, 2016
PubMed
Summary
This summary is machine-generated.

Oncogenic transformation generates microvesicles (MVs) containing focal adhesion kinase, promoting cancer cell survival and growth. Inhibiting this kinase in MVs reverses these effects, suggesting MVs as potential cancer markers.

Keywords:
PTK2 protein tyrosine kinase 2 (PTK2)cell signalingexosome (vesicle)extracellular vesiclesfocal adhesion kinase (FAK)intercellular communicationmicroparticlesmicrovesiclestransformation

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Area of Science:

  • Cell Biology
  • Cancer Research
  • Biochemistry

Background:

  • Extracellular vesicles (EVs), including exosomes and microvesicles (MVs), are key mediators of intercellular communication.
  • EVs from cancer cells influence cancer progression by transferring proteins and RNA.
  • The impact of oncogenic transformation on EV biogenesis and function requires further elucidation.

Purpose of the Study:

  • To investigate how oncogenic transformation affects microvesicle (MV) biogenesis and function.
  • To identify specific molecular cargo within MVs that contributes to cancer progression.
  • To explore the potential of these MVs as diagnostic markers for malignant disease.

Main Methods:

  • Utilized a mouse embryonic fibroblast (MEF) cell line inducible for oncogenic diffuse B cell lymphoma (Dbl) expression.
  • Analyzed microvesicles (MVs) isolated from both oncogenic and control MEFs for protein content.
  • Assessed the functional impact of MVs on fibroblast survival and anchorage-independent growth, employing genetic knockdown and pharmacological inhibition of focal adhesion kinase (FAK).

Main Results:

  • Microvesicles (MVs) from oncogenic Dbl-expressing MEFs contained focal adhesion kinase (FAK), unlike those from control cells.
  • Addition of these FAK-containing MVs promoted fibroblast survival and anchorage-independent growth.
  • These pro-cancer effects were reversed by FAK knockdown, FAK depletion from MVs, or FAK kinase inhibition, and were also observed with MVs from MDAMB231 breast cancer cells.

Conclusions:

  • Oncogenic transformation induces the production of microvesicles (MVs) uniquely enriched with focal adhesion kinase (FAK).
  • FAK within MVs propagates the transformed phenotype by enhancing cell survival and anchorage-independent growth.
  • These FAK-carrying MVs represent a potential diagnostic marker for malignant diseases.