Related Experiment Video

Updated: Jan 13, 2026

Coculture Assays to Study Macrophage and Microglia Stimulation of Glioblastoma Invasion
09:23

Coculture Assays to Study Macrophage and Microglia Stimulation of Glioblastoma Invasion

Published on: October 20, 2016

14.7K

METTL3 abrogation promotes glioma progression through regulating the ISG15-FASN axis-mediated lipid metabolism in

Huilong Yin1,2,3,4,5, Xiaoyi Yu6,7,8, Chenglong Hu6,7,8

  • 1Henan Key Laboratory of Immunology and Targeted Therapy, School of Medical Technology, Xinxiang Medical University, Xinxiang, Henan, China. hlyin@xxmu.edu.cn.

Nature Communications
|January 8, 2026
PubMed

Insights

The m6A methyltransferase METTL3 regulates macrophage metabolism in glioblastoma (GBM). METTL3 deficiency enhances lipid metabolism and impairs anti-tumor immunity, offering potential therapeutic targets for GBM.

Area of Science:

  • Immunology
  • Cancer Biology
  • Epigenetics

Background:

  • Tumor-associated macrophages (TAMs) are key in the tumor microenvironment.
  • The role of N6-methyladenosine (m6A) in TAM metabolism is unclear.

Purpose of the Study:

  • Investigate the link between m6A and TAM metabolic patterns.
  • Determine METTL3's function in glioblastoma (GBM) macrophages.

Main Methods:

  • Analyzed monocyte-derived macrophages from GBM patients.
  • Utilized conditional knockout of Mettl3 in myeloid cells.
  • Assessed lipid metabolism, CD8+ T cell response, and FASN expression.

Main Results:

  • METTL3 is downregulated in GBM TAMs.
  • Mettl3 deficiency increases lipid metabolism and accelerates glioma.
  • METTL3 deficiency upregulates FASN via ISG15, impairing CD8+ T cell function.
  • Targeting FASN or ISG15 reverses tumor progression.

Conclusions:

  • m6A modification is crucial for regulating TAM metabolism.
  • METTL3-ISG15-FASN axis impacts GBM progression and anti-tumor immunity.
  • FASN represents a potential therapeutic target for GBM.

More Related Videos

Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections05:45

Quantitative Immunohistochemistry of the Cellular Microenvironment in Patient Glioblastoma Resections

Published on: July 31, 2017

10.1K
Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells12:52

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

Published on: November 28, 2015

16.4K

Related Concept Videos

mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
4.6K
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
5.1K
PI3K/mTOR/AKT Signaling Pathway01:22

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...
5.3K