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Published on: July 31, 2017
Hypoxia-Activated PERK Promotes Epithelial-Mesenchymal Transition in Gliomas: A Single-Cell and Spatial
Jingyan Gu1,2, Yue Kong3, Yaohua Liu1,2
1Department of Neurosurgery, Shanghai General Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai Jiao Tong University, 200080 Shanghai, China.
Hypoxia activates the PKR-like endoplasmic reticulum kinase (PERK) pathway, promoting glioma cell invasion and tumor growth. Targeting PERK or SPP1-CD44 interactions may offer new treatments for aggressive gliomas.
Area of Science:
- Neuro-oncology
- Cancer Biology
- Molecular Biology
Background:
- Glioma, a common adult brain tumor, is characterized by hypoxia and invasiveness.
- Endoplasmic reticulum stress (ERS) and the unfolded protein response (UPR) are linked to tumor progression.
- Epithelial mesenchymal transition (EMT) drives glioma invasion and metastasis.
Purpose of the Study:
- To investigate the role of ERS, specifically the PKR-like endoplasmic reticulum kinase (PERK) pathway, in promoting EMT and malignancy in glioma.
- To analyze PERK activity in high-grade and hypoxic gliomas using transcriptomic data.
- To evaluate the correlation between PERK activation and EMT upregulation.
Main Methods:
- Analysis of bulk and single-cell transcriptomic data to assess PERK activity and EMT correlation.
- Investigation of PERK's effects on glioma migration and invasion in hypoxic conditions using PERK-silenced cell lines.
- In vivo assessment of tumorigenicity and evaluation of intercellular communication and spatial transcriptomics.
Main Results:
- Hypoxia-induced PERK activation enhanced glioma cell migration, invasion, and tumor growth by promoting EMT.
- High PERK signatures correlated with EMT activation in aggressive gliomas.
- PERK inhibition reduced tumor size, and PERK-activated cells showed increased SPP1-CD44 interactions within hypoxic niches.
Conclusions:
- PERK-driven EMT is a key mechanism linking ER stress to glioma progression, reinforced by hypoxia.
- Targeting the PERK signaling axis or SPP1-CD44 interactions presents potential therapeutic strategies for aggressive gliomas.
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