Journal
JOURNAL OF CLINICAL PATHOLOGY
Volume 69, Issue 2, Pages 171-175Publisher
BMJ PUBLISHING GROUP
DOI: 10.1136/jclinpath-2015-203125
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Funding
- Biotechnology and Biological Sciences Research Council [BB/J007293/1]
- Richard Bright VEGF Research Trust
- Biotechnology and Biological Sciences Research Council [BB/J007293/2, BB/P012035/1, BB/J007293/1] Funding Source: researchfish
- British Heart Foundation [PG/15/53/31371] Funding Source: researchfish
- Medical Research Council [G1002073] Funding Source: researchfish
- BBSRC [BB/J007293/2, BB/J007293/1, BB/P012035/1] Funding Source: UKRI
- MRC [G1002073] Funding Source: UKRI
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Vascular endothelial growth factor (VEGF) undergoes alternative splicing to produce both proangiogenic and antiangiogenic isoforms. Preferential splicing of proangiogenic VEGF is determined by serine-arginine protein kinase 1 (SRPK1), which is upregulated in a number of cancers. In the present study, we aimed to investigate SRPK1 expression in prostate cancer (PCa) and its association with cancer progression. SRPK1 expression was assessed using immunohistochemistry of PCa tissue extracted from radical prostatectomy specimens of 110 patients. SRPK1 expression was significantly higher in tumour compared with benign tissue (p < 0.00001) and correlated with higher pT stage (p = 0.004), extracapsular extension (p = 0.003) and extracapsular perineural invasion (p = 0.008). Interestingly, the expression did not correlate with Gleason grade (p = 0.21), suggesting that SRPK1 facilitates the development of a tumour microenvironment that favours growth and invasion (possibly through stimulating angiogenesis) while having little bearing on the morphology or function of the tumour cells themselves.
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