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Shutting Down the 'Language Encoder': A Pathogen-Derived Nano-Interferer Disrupt Sialylation Metabolism and Reprogram

Jingyi Zhou1, Zonghua Tian1, Yun Chen1

  • 1Department of Pharmaceutics, School of Pharmaceutical Sciences, Fudan University, Key Laboratory of Smart Drug Delivery, Ministry of Education, State Key Laboratory of Brain Function and Disorders, MOE Frontiers Center for Brain Science, Shanghai, 201203, China.

Advanced Materials (Deerfield Beach, Fla.)
|November 29, 2025
PubMed
Summary

Researchers developed a novel nano-interferer (OMV@HM-T/F) to target glioblastoma (GBM). This strategy remodels cancer cell communication by inhibiting sialylation, offering a new approach to combat GBM

Keywords:
bacterial outer membraneimmune modulationintercellular communicationmembrane proteinsmetabolic regulationnano‐interferer, sialylation

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Area of Science:

  • Neuro-oncology
  • Glycobiology
  • Nanomedicine

Background:

  • Glioblastoma (GBM) exhibits high adaptability and therapeutic resistance due to a communication network facilitated by enhanced membrane protein sialylation.
  • This metabolism-driven network supports malignant phenotypes within the restrictive cranial space and blood-brain barrier (BBB).
  • Effective GBM treatment is challenged by the blood-brain barrier and tumor's adaptive nature.

Purpose of the Study:

  • To propose and develop a "metabolism-guided decoding of communication architecture" strategy for GBM.
  • To create a brain-targeted nano-interferer capable of disrupting GBM's communication pathways.
  • To investigate a novel approach for overcoming therapeutic resistance in glioblastoma.

Main Methods:

  • Development of a pathogen-derived nano-interferer (OMV@HM-T/F) designed for brain targeting.
  • Simultaneous inhibition of glycosylation precursor synthesis and sialic acid activation.
  • Integration of blood-brain barrier penetrability and tumor microenvironment responsiveness in the nano-interferer.

Main Results:

  • The OMV@HM-T/F platform effectively remodels membrane glycan structures in GBM.
  • Disruption of glycan-dependent communication scaffolds and downstream signaling pathways was observed.
  • Inhibition of immune suppression pathways and enhancement of therapeutic efficacy are indicated.

Conclusions:

  • The "metabolism-guided decoding of communication architecture" strategy offers precise metabolic-level intervention in GBM.
  • The developed nano-interferer (OMV@HM-T/F) shows promise in overcoming GBM's high adaptability and therapeutic resistance.
  • This approach provides a novel therapeutic avenue for treating glioblastoma by targeting its fundamental communication mechanisms.