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SRSF3 Depletion Leads to an Increase in SF3B4 Expression in SNU-368 HCC Cells
Jeehan Lee1,2,3, Gwanwoo Seo1,2, Wonhee Hur4
1Department of Biochemistry, The Catholic University of Korea, Seoul, Republic of Korea.
Background:
SF3B4, a critical component of U2 pre-mRNA spliceosomal complex, has been recently indicated as a potential oncogene in hepatocellular carcinoma (HCC). However, limited information exists on how SF3B4 expression is regulated in HCC.
Materials And Methods:
To determine the regulatory factor for SF3B4 expression, small interfering RNA (siRNA), real-time polymerase chain reaction (qRT-PCR) and western blotting assay were performed. The in vivo expression profiles of SRSF3 and SF3B4 were analyzed using public datasets and clinical samples.
Results:
Among 10 liver-specific splicing factors, only SRSF3 knockdown resulted in a significant increase in SF3B4 mRNA and consequently protein levels in SNU-368 HCC cells, probably via the retardation of SF3B4 mRNA decay rates. Using green fluorescent protein-SF3B4 fusion construct, the coding region of SF3B4 was found to be involved in SRSF3-mediated regulation of SF3B4 expression. Publicly available data from paired normal and tumor tissues in HCC and results from patients with HCC suggest that SRSF3 and SF3B4 possess an inverse relationship.
Conclusion:
SRSF3 is a key molecule for determining SF3B4 levels in HCC cells.
