scholarly journals All-trans retinoic acid reverses epithelial-mesenchymal transition in paclitaxel-resistant cells by inhibiting nuclear factor kappa B and upregulating gap junctions

2018 ◽  
Vol 110 (1) ◽  
pp. 379-388 ◽  
Author(s):  
Guiling Shi ◽  
Xiaoli Zheng ◽  
Xiaojing Wu ◽  
Siqi Wang ◽  
Yijia Wang ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Gap Junctions ◽  
Nuclear Factor Kappa B ◽  
Epithelial Mesenchymal Transition ◽  
Nuclear Factor ◽  
Mesenchymal Transition ◽  
Nuclear Factor Kappa ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Resistant Cells

scholarly journals FABP5 enhances malignancies of lower-grade gliomas via canonical activation of NF-κB signaling

2020 ◽  
Author(s):  
Jia Wang ◽  
Wahafu Alafate ◽  
Yichang Wang ◽  
Wei Wu ◽  
Jianyang Xiang ◽  
...  
Keyword(s):  
Nuclear Factor Kappa B ◽  
Epithelial Mesenchymal Transition ◽  
Lower Grade ◽  
Nuclear Factor ◽  
Fatty Acid Binding ◽  
Mesenchymal Transition ◽  
Molecular Stratification ◽  
Nuclear Factor Kappa ◽  
Grade Ii ◽  
Factor Α

Abstract Background Lower-grade gliomas (LGGs) are grade II/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 remain poor. Methods In this study, we derived all relevant data of LGGs including TCGA and CGGA databases from official websites. Bioinformatic analyses unveiled the clinical significance of FABP5 and its potential downstream targets. IHC, qRT-PCR and western blot assays were further conducted to validate those bioinformatic findings. Moreover, lentiviral transduction assays were performed to evaluate the function of FABP5 in patient-derived cell lines. Results 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, migration, 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 tumor necrosis factor α (TNFα)-dependent NF-κB signaling 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) signaling. Conclusion Taken together, our study indicated that FABP5 enhances malignancies of LGGs through canonical activation of NF-κB signaling, which could be used as individualized prognostic biomarker and potential therapeutic target of LGGs.

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