Background: Our previous study demonstrated that Myosin Phosphatase
Targeting subunit 1 (MYPT1) may function as a direct target of microRNA-30d, which
promotes tumor angiogenesis and tumor growth of prostate cancer (PCa). Here, we
aimed to investigate the clinical significance of MYPT1 expression and its functions in
Methods: Roles of MYPT1 deregulation in tumor angiogenesis of PCa was determined
in vitro and in vivo experiments. Expression patterns of MYPT1 and CD31 proteins were
examined by immunohistochemistry and immunofluorescence, respectively.
Associations of MYPT1/CD31 combination with various clinicopathological features and
patients' prognosis of PCa were also statistically evaluated.
Results: Through gain- and loss-of-function experiments, MYPT1 inhibited capillary
tube formation of endothelial cells and in vivo tumor angiogenesis in a mouse model with
the downregulation of VEGF and CD31 expression. In addition, MYPT1 expression was
significantly decreased, while CD31 expression was dramatically increased in PCa
tissues compared to benign prostate tissues. Notably, MYPT1 expression levels in PCa
tissues were negatively correlated with that of CD31. Statistically, MYPT1-low/CD31-
high expression was distinctly associated with high Gleason score, positive biochemical
recurrence, and reduced overall survival of PCa patients. Moreover, PCa patients with
MYPT1-low/CD31-high expression more frequently had shorter overall, biochemical
recurrence-free and metastasis-free survivals. MYPT1/CD31 combination was identified
as an independent factor to predict biochemical recurrence-free and metastasis-free
survivals of PCa patients.
Conclusions: Our findings indicate that MYPT1 may inhibit angiogenesis and contribute
favorable prognosis in PCa patients, implying that MYPT1 might be a potential drug
candidate in anticancer therapy.