The effect of ALKBH5 overexpression on gene expression in the Huh-7 cell line

Huh-7 is a sorafenib-sensitive hepatocellular carcinoma cell line. Short-term exposure (48 hours) of Huh-7 cells to sorafenib induces transcriptome-wide m6A hypomethylation and specifically upregulates the expression of the m6A demethylase ALKBH5. Functional analyses demonstrate that ALKBH5 overexpression promotes cellular resistance to sorafenib. To elucidate the molecular mechanisms by which ALKBH5 triggers sorafenib resistance in Huh-7 cells, we performed RNA sequencing (RNA-seq) on ALKBH5-overexpressing Huh-7 cells. RNA-seq data analysis revealed that ALKBH5 overexpression enhances the expression of epithelial-mesenchymal transition (EMT)-related genes and upregulates genes associated with the Wnt/ß-catenin signaling pathway. Overall design: RNA-seq profiling of parental Huh7 cells and ALKBH5-overexpressing counterparts

Huh-7是索拉非尼敏感的肝细胞癌细胞系。将Huh-7细胞短期暴露于索拉非尼48小时，可诱导全转录组范围内的m⁶A低甲基化，并特异性上调m⁶A去甲基化酶ALKBH5的表达。功能分析结果显示，ALKBH5过表达可促进细胞对索拉非尼的耐药性。为阐明ALKBH5介导Huh-7细胞产生索拉非尼耐药的分子机制，我们对过表达ALKBH5的Huh-7细胞进行了RNA测序（RNA-seq）。RNA-seq数据分析表明，ALKBH5过表达可增强上皮间质转化（epithelial-mesenchymal transition，EMT）相关基因的表达，并上调与Wnt/β-连环蛋白（Wnt/β-catenin）信号通路相关的基因。整体实验设计：亲本Huh7细胞与过表达ALKBH5的对应细胞的RNA-seq图谱分析