FABP5 enhances malignancies of lower‐grade gliomas via canonical activation of NF‐κB signaling
| Autor: | Dongze Xu, Yichang Wang, Xudong Ma, Xiaobin Bai, Maode Wang, Wanfu Xie, Wei Wu, Alafate Wahafu, Jia Wang, Longwei Huo, Ning Wang, Hao Liu, Jianyang Xiang |
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| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Necrosis FABP5 Apoptosis Fatty Acid-Binding Proteins Malignancy Fatty acid-binding protein 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Biomarkers Tumor Tumor Cells Cultured medicine Humans Neoplasm Invasiveness tumour recurrence Cell Proliferation Wound Healing Brain Neoplasms Chemistry Kinase Genetic heterogeneity NF‐κB NF-kappa B NF-κB Original Articles Glioma Cell Biology Prognosis medicine.disease Gene Expression Regulation Neoplastic Survival Rate 030104 developmental biology lower‐grade glioma 030220 oncology & carcinogenesis Cancer research Molecular Medicine Phosphorylation Original Article Tumor necrosis factor alpha medicine.symptom malignancy Signal Transduction |
| Zdroj: | Journal of Cellular and Molecular Medicine |
| ISSN: | 1582-4934 1582-1838 |
| Popis: | Low‐grade gliomas (LGGs) are grade III gliomas based on the WHO classification with significant genetic heterogeneity and clinical properties. Traditional histological classification of gliomas has been challenged by the improvement of molecular stratification; however, the reproducibility and diagnostic accuracy of LGGs classification still remain poor. Herein, we identified fatty acid binding protein 5 (FABP5) as one of the most enriched genes in malignant LGGs and elevated FABP5 revealed severe outcomes in LGGs. Functionally, lentiviral suppression of FABP5 reduced malignant characters including proliferation, cloning formation, immigration, invasion and TMZ resistance, contrarily, the malignancies of LGGs were enhanced by exogenous overexpression of FABP5. Mechanistically, epithelial‐mesenchymal transition (EMT) was correlated to FABP5 expression in LGGs and tumour necrosis factor α (TNFα)‐dependent NF‐κB signalling was involved in this process. Furthermore, FABP5 induced phosphorylation of inhibitor of nuclear factor kappa‐B kinase α (IKKα) thus activated nuclear factor kappa‐B (NF‐κB) signalling. Taken together, our study indicated that FABP5 enhances malignancies of LGGs through canonical activation of NF‐κB signalling, which could be used as individualized prognostic biomarker and potential therapeutic target of LGGs. |
| Databáze: | OpenAIRE |
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