Effect of overexpression of NFAT5 on gene expression during TMZ resistance of U87 and U251 cells.
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ABSTRACT:
PROVIDER: PRJNA898426 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22197549.fastq.gz | Fastqsanger.gz | |||
| SRR22197550.fastq.gz | Fastqsanger.gz | |||
| SRR22197551.fastq.gz | Fastqsanger.gz | |||
| SRR22197552.fastq.gz | Fastqsanger.gz | |||
| SRR22197553.fastq.gz | Fastqsanger.gz |
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Project description:We present RNA-Seq data obtained from U251 control cells and U251 cells with stable overexpression of lncRNA XLOC13218 to identify differentially expressed genes. The discovery of long non-coding RNAs (lncRNAs) has improved the understanding of development and progression in various cancer sub-types. However, the role of lncRNAs in temozolomide (TMZ) resistance in glioblastoma (GBM) remains largely undefined. In this present study, the differential expression of lncRNAs were identified between U87 and U87TR (TMZ-resistant) cells. LncRNA XLOC013218 (XLOC) was drastically upregulated in TMZ-resistant cells and was associated with poor prognosis in glioma. Overexpression of XLOC markedly increased TMZ resistance, promoted proliferation, and inhibited apoptosis in vitro and in vivo. In addition, RNA-seq analysis and gain-of-function or loss-of-function studies revealed that PIK3R2 was the potential target of XLOC. Mechanistically, XLOC recruited Specificity Protein 1 (Sp1) transcription factor and promoted the binding of Sp1 to the promoters of PIK3R2, which elevated the expression of PIK3R2 in both mRNA and protein levels. Finally, PIK3R2-mediated activation of the PI3K/AKT signaling pathway promoted TMZ resistance and cell proliferation, but inhibited cell apoptosis. In conclusion, these data highlight the vital role of XLOC/Sp1/PIK3R2/PI3K/AKT axis in GBM TMZ resistance.
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