Effects of Nogo-B receptor overexpression on transcriptomic profiling in the NIH3T3 fibroblast cell line
Unrestrained receptor tyrosine kinase (RTK) signaling and epigenetic dysregulation are responsible in part for tumorigenesis. Aberrant RTK signaling results in the remodeling of histone modification. As a Ras modulator, NgBR promotes Ras-mediated RTK signaling pathways. Meanwhile, we observed that NgBR overexpression in NIH3T3 cells significantly increased the acetylation of histone H3 and histone H4. To further elucidate the underlying mechanism that NgBR upregulates histone acetylation in tumorigenesis, we carried out RNA-seq analysis to examine the transcriptome alternation in NIH3T3 cells and NgBR-overexpressed NIH3T3 cells (3T3NgBR cells) and revealed that overexpression of NgBR up-regulates ACSS2 expression, but not ACSS1 and ACSS3. Moreover. ACSS2 overexpression abrogated NgBR deficiency-caused decrease of histone acetylation in NIH3T3 cells. Taken together, all the data suggested that NgBR regulates tumorigenesis in NIH3T3 cells via ACSS2-mediated histone acetylation. Overall design: Comparative gene expression analysis of RNASeq data for NIH3T3 cells (wild type) and NgBR overexpressed NIH3T3 cell (3T3NgBR).