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Characterization of Immune Cell-derived Extracellular Vesicles and Studying Functional Impact on Cell Environment
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Characterization of Immune Cell-derived Extracellular Vesicles and Studying Functional Impact on Cell Environment

Published on: June 2, 2020

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Extracellular Vesicle lncRNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 Released From Glioma Stem Cells

Jiankai Yang1, Guozhu Sun1, Yuhua Hu1

  • 1Department of Neurosurgery, The Second Hospital of Hebei Medical University, Shijiazhuang, China.

Frontiers in Immunology
|March 3, 2020
PubMed

Insights

Glioma stem cell extracellular vesicles (EVs) carrying MALAT1 influence microglia inflammation. This involves regulating the miR-129-5p/HMGB1 pathway, impacting cytokine release and glioma progression.

Area of Science:

  • Neuro-oncology
  • Cellular Biology
  • Molecular Biology

Background:

  • Glioma stem cells (GSCs) communicate with microglia via extracellular vesicles (EVs).
  • Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a long non-coding RNA, plays a role in cancer progression.
  • Microglia activation contributes to the tumor microenvironment in glioma.

Purpose of the Study:

  • To investigate the role of GSC-derived EVs and MALAT1 in modulating microglia inflammatory responses.
  • To elucidate the molecular mechanism involving MALAT1, miR-129-5p, and HMGB1 in GSC-microglia communication.

Main Methods:

  • Real-time PCR to detect MALAT1 expression in GSCs, EVs, and microglia.
  • Luciferase reporter assays to confirm targeting interactions between MALAT1, miR-129-5p, and HMGB1.
  • Analysis of inflammatory cytokine (IL-6, IL-8, TNF-α) expression and secretion in microglia under various experimental conditions, including EV exposure and genetic manipulation.

Main Results:

  • MALAT1 was significantly enriched in GSC-derived EVs and upregulated in microglia upon EV incubation.
  • GSC EVs, particularly those containing MALAT1, exacerbated inflammatory responses in lipopolysaccharide-stimulated microglia.
  • MALAT1 directly targets miR-129-5p, which in turn targets HMGB1, establishing a regulatory axis (MALAT1/miR-129-5p/HMGB1) that influences microglia inflammation.

Conclusions:

  • GSC-derived EVs carrying MALAT1 promote microglia inflammatory responses through the miR-129-5p/HMGB1 axis.
  • Targeting MALAT1 in GSCs or inhibiting EV secretion may offer therapeutic strategies for glioma by modulating neuroinflammation.
Keywords:
extracellular vesicleshigh mobility group box-1 protein (HMGB1)metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)miR-129-5pmicroglia

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