Abstract
Serine-arginine protein kinase 1 (SRPK1) phosphorylates proteins involved in the regulation of several mRNA-processing pathways, including alternative splicing. SRPK1 has been recently reported to be overexpressed in multiple cancers, including prostate cancer, breast cancer, lung cancer, and glioma. Several studies have shown that inhibition of SRPK1 has anti-tumoural effects, and SRPK1 has therefore become a new candidate for targeted therapies. Interestingly, in terms of molecular mechanism, SRPK1 seems to act heterogeneously, and has been reported to affect several processes in different cancers, e.g. angiogenesis in prostate and colon cancer, apoptosis in breast and colon cancer, and migration in breast cancer. A recent report adds to this puzzle, showing that the main effect of SRPK1 overexpression in non-small-cell lung carcinoma is to stimulate a stem cell-like phenotype. This pleiotropy might be related to preferential activation of different downstream signalling pathways by SRPK1 in various cancers. © 2016 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.