ArticleScientific reports2015
PERK silence inhibits glioma cell growth under low glucose stress by blockage of p-AKT and subsequent HK2's mitochondria translocation.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- Systematic Review of Molecular Targeted Therapies for Adult-Type Diffuse Glioma: An Analysis of Clinical and Laboratory Studies.International journal of molecular sciences · 2023Pooled it
- Review
- MiR-204-5p mediates PERK inhibition to suppress growth and induce apoptosis in ovarian cancer through the eIF2α/ATF-4/CHOP pathway.Scientific reports · 2025Article
- The unfolded protein response machinery in glioblastoma genesis, chemoresistance and as a druggable target.CNS neuroscience & therapeutics · 2024Review
- Heparanase interacting BCLAF1 to promote the development and drug resistance of ICC through the PERK/eIF2α pathway.Cancer gene therapy · 2024Article
- Glucose-driven histone lactylation promotes the immunosuppressive activity of monocyte-derived macrophages in glioblastoma.Immunity · 2024Article
- DNA Damage-Induced Apoptosis Suppressor Triggers Progression and Stemness of Glioma by Enhancing Lymphoid Enhancer-Binding Factor 1 Expression.World journal of oncology · 2024Article
- Endoplasmic Reticulum Stress in the Brain Tumor Immune Microenvironment.Molecular cancer research : MCR · 2023Article
- Aiding Cancer's "Sweet Tooth": Role of Hexokinases in Metabolic Reprogramming.Life (Basel, Switzerland) · 2023Review
- Cerebral Glucose Metabolism and Potential Effects on Endoplasmic Reticulum Stress in Stroke.Aging and disease · 2023Review
- DNMT2/TRDMT1 gene knockout compromises doxorubicin-induced unfolded protein response and sensitizes cancer cells to ER stress-induced apoptosis.Apoptosis : an international journal on programmed cell death · 2023Article
- Classification related to immunogenic cell death predicts prognosis, immune microenvironment characteristics, and response to immunotherapy in lower-grade gliomas.Frontiers in immunology · 2023Article
- Integrative analysis defines DDIT3 amplification as a correlative and essential factor for glioma malignancy.American journal of cancer research · 2023Article
- Neuron-specific translational control shift ensures proteostatic resilience during ER stress.The EMBO journal · 2022Article
- Morusin Enhances Temozolomide Efficiency in GBM by Inducing Cytoplasmic Vacuolization and Endoplasmic Reticulum Stress.Journal of clinical medicine · 2022Article
- A DNA repair-independent role for alkyladenine DNA glycosylase in alkylation-induced unfolded protein response.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Heterogeneity of glioblastoma stem cells in the context of the immune microenvironment and geospatial organization.Frontiers in oncology · 2022Review
- Unconventional Protein Secretion in Brain Tumors Biology: Enlightening the Mechanisms for Tumor Survival and Progression.Frontiers in cell and developmental biology · 2022Review
- Current Development and Application of Anaerobic Glycolytic Enzymes in Urothelial Cancer.International journal of molecular sciences · 2021Review
- Endoplasmic Reticulum Stress Contributes to Gefitinib-Induced Apoptosis in Glioma.International journal of molecular sciences · 2021Article
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Authors and funding
20 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioma relies on glycolysis to obtain energy and sustain its survival under low glucose microenvironment in vivo. The mechanisms on glioma cell glycolysis regulation are still unclear. Signaling mediated by Double-stranded RNA-activated protein kinase (PKR) - like ER kinase (PERK) is one of the important pathways of unfolded protein response (UPR) which is comprehensively activated in cancer cells upon the hypoxic and low glucose stress. Here we show that PERK is significantly activated in human glioma tissues. PERK silencing results in decreased glioma cell viability and ATP/lactate production upon low glucose stress, which is mediated by partially blocked AKT activation and subsequent inhibition of Hexokinase II (HK2)'s mitochondria translocation. More importantly, PERK silenced glioma cells show decreased tumor formation capacity. Our results reveal that PERK activation is involved in glioma glycolysis regulation and may be a potential molecular target for glioma treatment.
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