Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

PI3K/mTOR/AKT Signaling Pathway

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Experiences of racially, ethnically, sexual- and gender-minoritized adolescents and young adults with cancer in the Canadian health care system.

Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer·2026

Same author

SIRT2 mediates integrated stress response by deacetylating and stabilizing 4E-BP1 to suppress translation.

EMBO reports·2026

Same author

Structure and enzymology of glutaminase S482C and H461L variants associated with excess brain glutamate and neurological disease.

The Journal of biological chemistry·2026

Same author

A highly dynamic active state for transducin-bound phosphodiesterase-6 in vertebrate phototransduction.

bioRxiv : the preprint server for biology·2026

Same author

Diverse microbial exposure exacerbates the development of allergic airway inflammation in adult mice.

Journal of immunology (Baltimore, Md. : 1950)·2026

Same author

Sulfur-containing class of broad-spectrum antivirals improves influenza virus vaccine development.

Nature communications·2026

Search research articles

Related Experiment Video

Updated: Jun 4, 2025

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice

Published on: August 12, 2014

PTEN loss in glioma cell lines leads to increased extracellular vesicle biogenesis and PD-L1 cargo in a

Julio C Sanchez¹, Timothy M Pierpont², Dariana Argueta-Zamora¹

¹Department of Molecular Medicine, College of Veterinary Medicine, Cornell University, Ithaca, New York, USA.

The Journal of Biological Chemistry

|December 28, 2024

Summary

This summary is machine-generated.

Loss of the tumor suppressor Phosphatase and Tensin Homolog (PTEN) enhances extracellular vesicle (EV) production and PD-L1 loading. These PTEN-deficient EVs suppress T cell signaling, impacting the tumor immune microenvironment.

Keywords:

Glioblastoma extracellular vesicles immunosuppression phosphatase and tensin homolog (PTEN)phosphatidylinositide 3-kinase (PI 3-kinase)

More Related Videos

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells

Published on: November 28, 2015

Transposon Mediated Integration of Plasmid DNA into the Subventricular Zone of Neonatal Mice to Generate Novel Models of Glioblastoma

Transposon Mediated Integration of Plasmid DNA into the Subventricular Zone of Neonatal Mice to Generate Novel Models of Glioblastoma

Published on: February 22, 2015

Related Experiment Videos

Last Updated: Jun 4, 2025

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice

Published on: August 12, 2014

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells

Published on: November 28, 2015

Transposon Mediated Integration of Plasmid DNA into the Subventricular Zone of Neonatal Mice to Generate Novel Models of Glioblastoma

Transposon Mediated Integration of Plasmid DNA into the Subventricular Zone of Neonatal Mice to Generate Novel Models of Glioblastoma

Published on: February 22, 2015

Area of Science:

Oncology
Immunology
Cell Biology

Background:

Phosphatase and Tensin Homolog (PTEN) is a critical tumor suppressor and regulator of the PI3K-AKT pathway.
Loss of PTEN is linked to immune suppression, increased PD-L1 expression, and resistance to immunotherapy.
Extracellular vesicles (EVs) play roles in intercellular communication and immune modulation.

Purpose of the Study:

To investigate how PTEN loss affects EV biogenesis, cargo, and function, particularly PD-L1 content.
To determine the role of PI3K signaling in PTEN-loss-mediated changes in EVs.
To assess the impact of PTEN-deficient EVs on T cell receptor signaling.

Main Methods:

Genetic and pharmacological manipulation of PTEN expression in cancer cells.
Analysis of PD-L1 expression and localization.
Characterization of EV biogenesis and cargo enrichment.
Assessment of T cell suppression assays.

Main Results:

PTEN loss upregulates cell surface PD-L1 via JAK/STAT signaling, but enhances EV biogenesis and PD-L1 loading in a PI3K-dependent manner.
EVs derived from PTEN-deficient cells exhibit increased PD-L1 content.
These EVs demonstrate enhanced suppression of T cell receptor signaling.

Conclusions:

PTEN loss promotes an immunosuppressive tumor microenvironment through PI3K-dependent regulation of PD-L1-enriched EVs.
This study reveals a novel role for PI3K signaling in EV biogenesis and cargo selection.
Findings offer insights into immune evasion mechanisms and potential therapeutic strategies targeting PTEN-deficient tumors.