The aberrant upregulation of exon 10-inclusive SREK1 through SRSF10 acts as an oncogenic driver in human hepatocellular carcinoma

The deregulation of alternative splicing (AS) has recently been implicated as a relevant source of molecular heterogeneity in cancer. However, the targets and intrinsic mechanisms on regulatory network of splicing in hepatocarcinogenesis are largely unknown. Here, we report a functional impact of the splice variant of Splicing Regulatory Glutamic Acid and Lysine Rich Protein 1 (SREK1) and its upstream regulator, Serine/arginine-rich splicing factor 10 (SRSF10) on sustaining the oncogenic signal.