Non-canonical splice variant of PFKFB4 in hepatocellular carcinoma activates AKT through direct interaction.

ABSTRACT:

Background & aims

The glycolytic enzyme 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 4 (PFKFB4) has emerged as a vital oncogene in many cancer types as a result of its metabolic function and signaling pathways. However, the effects of alternative splicing variants of PFKFB4 remain largely unexplored.

Methods

Clinical hepatocellular carcinoma (HCC) specimens were used to established the clinical implications of PFKFB4 variants. HCC cell lines and xenograft models were applied to characterize the function of PFKFB4 variants. The underlying mechanisms involved were investigated through the use of human proteome phosphate arrays, in vitro kinase assays, and immunoprecipitation.

Results

We identified a previously uncharacterized splicing variant of PFKFB4<

SUBMITTER: Wan HL 

PROVIDER: S-EPMC12639319 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature