MFAP2 Promotes Glioblastoma Malignant Phenotypes via Autophagy-Dependent Activation of Wnt/β-Catenin Signaling

Peihao Yang1, Demeng Liu1, Jiyao Wang2

  • 1Department of Pharmacy, The Second Affiliated Hospital of Zhengzhou University, Academy of Medical Sciences, Zhengzhou University, Zhengzhou 450053, China.

Biomedicines
|May 27, 2026
PubMed

Insights

Microfibrillar-associated protein 2 (MFAP2) drives glioblastoma growth by activating autophagy and Wnt/β-catenin signaling. MFAP2 is a potential prognostic biomarker and therapeutic target for glioblastoma (GBM).

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Signaling

Background:

  • Microfibrillar-associated protein 2 (MFAP2) is linked to cancers, but its role in glioblastoma (GBM) is unclear.
  • Understanding MFAP2's function is crucial for developing new GBM therapies.

Purpose of the Study:

  • To investigate the role and molecular mechanisms of MFAP2 in glioblastoma progression.
  • To evaluate MFAP2 as a potential prognostic biomarker and therapeutic target in GBM.

Main Methods:

  • Analyzed MFAP2 expression in clinical GBM samples and animal models.
  • Conducted in vitro gain/loss-of-function assays and in vivo orthotopic xenograft models.
  • Explored the interplay between autophagic flux and Wnt/β-catenin signaling pathways.

Main Results:

  • MFAP2 was overexpressed in GBM and correlated with poor prognosis.
  • MFAP2 enhanced GBM cell viability, migration, and invasion by activating autophagy and the Wnt/β-catenin pathway.
  • MFAP2 knockdown reduced tumor growth and suppressed the autophagy-Wnt axis in vivo.

Conclusions:

  • MFAP2 acts as an oncogenic driver in GBM, linking autophagy to Wnt/β-catenin signaling.
  • MFAP2 shows promise as a prognostic biomarker and therapeutic target for GBM.
  • Further validation in larger clinical cohorts and diverse GBM models is recommended.

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