A TNFR2-hnRNPK axis promotes primary liver cancer development via activation of YAP signaling in hepatic progenitor cells

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type, Tnfrsf1a-/- and Tnfrsf1ß-/- (with or without TNFa treat) HPCs Transcriptomes.The mRNA profiles of Wild Type, Tnfrsf1a-/- and Tnfrsf1ß-/- (with or without TNFa treat) HPCs were generated by deep sequencing, in triplicate, using Illumina GAIIx. The sequence reads that passed quality filters were analyzed at the transcript isoform level . qRT–PCR validation was performed using TaqMan and SYBR Green assays.We performed RNA-seq analysis to assess the global impacts of TNFR2 on HPCs' response to TNFa. Upon TNFa treatment, 519 genes were significantly upregulated in wild type HPCs . 39% of these genes (203 out of 519) were further upregulated in Tnfrsf1a-/- HPCs treated with TNFa. However, these 203 genes were dramatically downregulated in TNFa-treated Tnfrsf1b-/- HPCs relative to their expression in either TNFa-treated Tnfrsf1a-/- HPCs or wild type HPCs, indicating an inhibitory role for deletion of TNFR2 in the regulation of these genes. Overall design: Wild Type, Tnfrsf1a-/- and Tnfrsf1ß-/- (with or without TNFa treat) HPCs