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. To identify the alternative spliced targets of SRSF10 in HCC cells, we did the stable knockdown for the SRSF10 (3B-2, LM3-2) and Scramble control (3B-1, LM3-1) in Hep3B and HCCLM3 cells by lentivirus-mediated shRNA delivery. The RNA was extracted and sent for mRNA sequencing to identify the splicing targets regulated by SRSF10.