The lipid-lowering drug fenofibrate combined with si-HOTAIR can effectively inhibit the proliferation of gliomas

Background Fenofibrate is a fibric acid derivative known to have a lipid-lowering effect. Although fenofibrate-induced peroxisome proliferator-activated receptor alpha (PPAR[alpha]) transcription activation has been shown to play an important role in the malignant progression of gliomas, the underly...

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Published in:BMC cancer 2021-06, Vol.21 (1), p.1-664, Article 664
Main Authors: Zhu, Wei, Zhao, Hongyang, Xu, Fenfen, Huang, Bin, Dai, Xiaojing, Sun, Jikui, Nyalali, Alphonce M. K., Zhang, Kailiang, Ni, Shilei
Format: Article
Language:English
Subjects:
Angiogenesis
Antibodies
Antisense RNA
Apoptosis
Biological response modifiers
Brain cancer
Brain research
Cancer
Cell cycle
Cell growth
Cell lines
Cell proliferation
Drug therapy
Fenofibrate
Gene expression
Gene silencing
Genetic aspects
Genomes
Glioblastoma
Glioma
Glioma cells
Gliomas
Health aspects
HOTAIR
Lipids
Metabolism
Oncology, Experimental
Pathogenesis
PPARA
Proteins
Therapy
Transcription activation
Tumors
Wound healing
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Summary:Background Fenofibrate is a fibric acid derivative known to have a lipid-lowering effect. Although fenofibrate-induced peroxisome proliferator-activated receptor alpha (PPAR[alpha]) transcription activation has been shown to play an important role in the malignant progression of gliomas, the underlying mechanisms are poorly understood. Methods In this study, we analyzed TCGA database and found that there was a significant negative correlation between the long noncoding RNA (lncRNA) HOTAIR and PPAR[alpha]. Then, we explored the molecular mechanism by which lncRNA HOTAIR regulates PPAR[alpha] in cell lines in vitro and in a nude mouse glioma model in vivo and explored the effect of the combined application of HOTAIR knockdown and fenofibrate treatment on glioma invasion. Results For the first time, it was shown that after knockdown of the expression of HOTAIR in gliomas, the expression of PPAR[alpha] was significantly upregulated, and the invasion and proliferation ability of gliomas were obviously inhibited. Then, glioma cells were treated with both the PPAR[alpha] agonist fenofibrate and si-HOTAIR, and the results showed that the proliferation and invasion of glioma cells were significantly inhibited. Conclusions Our results suggest that HOTAIR can negatively regulate the expression of PPAR[alpha] and that the combination of fenofibrate and si-HOTAIR treatment can significantly inhibit the progression of gliomas. This introduces new ideas for the treatment of gliomas. Keywords: Glioblastoma, Fenofibrate, HOTAIR, PPARA, Therapy
ISSN:1471-2407
1471-2407
DOI:10.1186/s12885-021-08417-z