ENAapplication/xmlftp.sra.ebi.ac.uk/vol1/fastq/SRR137/022/SRR13777522/SRR13777522_1.fastq.gzftp.sra.ebi.ac.uk/vol1/fastq/SRR137/021/SRR13777521/SRR13777521_1.fastq.gzftp.sra.ebi.ac.uk/vol1/fastq/SRR137/023/SRR13777523/SRR13777523_1.fastq.gzftp.sra.ebi.ac.uk/vol1/fastq/SRR137/023/SRR13777523/SRR13777523_2.fastq.gzftp.sra.ebi.ac.uk/vol1/fastq/SRR137/022/SRR13777522/SRR13777522_2.fastq.gzftp.sra.ebi.ac.uk/vol1/fastq/SRR137/021/SRR13777521/SRR13777521_2.fastq.gzprimaryOK200GenomicsSouthern medical universityhttps://www.ebi.ac.uk/ena/browser/view/PRJNA704649Homo sapiensTo explore the mechanism by which PRMT7 regulates HCC cell malignant phenotypes, we performed RNA-seq in QGY-7703 cells before and after PRMT7 knockdown to identify the affected signaling pathways. 296 differentially expressed genes were identified in PRMT7-downregulated cells (Figure 6A) and these genes were enriched in cancer-related pathways including MAPK signaling pathway, p53 signaling pathway, and FoxO signaling pathway (Figure 6B), as revealed by DAVID KEGG analysis. Overall design: RNA-seq was constructed in QGY-7703 cells without PRMT7 knockdown and cells with PRMT7 knockdown by two short hairpin RNA (shRNA), shRNA1 and shRNA2, respectively.ENALine, RGD1304869, Whole Transcriptome Shotgun Sequencing, Cell Lines, BC006705, RNA-seq, Cell, 4933402B05Rik., LinesLine, RGD1304869, Whole Transcriptome Shotgun Sequencing, Cell Lines, BC006705, RNA-seq, Cell, 4933402B05Rik., Lines0.00.00.00.00.0falseRNA-seq in QGY-7703 cell line before and after PRMT7 knockdownRNA-seq in QGY-7703 cell line before and after PRMT7 knockdown2022-05-122021-02-27PRJNA704649GSE167432352645799606