Objective:To investigate the paired related homeobox 1 (PRRX1) and its pathway molecules expression in ovarian cancer and its relationship with the vasculogenic mimicry (VM) formation,so as to explore PRRX1 effect on metastasis and prognosis in ovarian cancer.Methods:The expressions of PRRX1,Wnt5a,β-catenin as well as VM in ovarian cancer samples from 62 cases were examined by immunohistochemical and C D31/periodic acid-Schiff double staining.And the relationships between PRRX 1 and VM formation,Wnt5a,β-catenin were assessed by x2 and pearson tests.The prognostic values of PRRX1 were measured by Kaplan-Meier survival analysis.Results:PRRX1 expression was associated with FIGO stage,metastasis and VM formation (P ＜0.05).No significant correlations were found between PRRX1 and age,tumor size,histological type,degree of differentiation of the tumor (P ＞0.05).PRRX1 overexpression was found to have the relationship with β-catenin nuclear expression but showed no relationship with Wnt5a and β-catenin cytoplasm expression.Both PRRX1 expression and VM formation were correlated with ovarian cancer metastasis and prognosis.Kaplan-Meier survival analysis showed that patients with PRRX1 expression and VM formation had shorter survival than PRRX1-or VM-patients,respectively.And poor prognosis was observed.PRRX1 expression and β-catenin nuclear expression had shorter survival than PRRX1-or β-catenin nuclear negative expression (P ＜0.05),where this relationship showed no significance between PRRX1 and Wnt5a,β-catenin cytoplasm expression (P ＞0.05).Conclusion:PRRX1 could regulate VM formation in ovarian cancer through the activation of Wnt/β-catenin signaling,indicating poor prognosis,so PRRX 1 might be a candidate marker for the diagnosis and prognosis predictor of ovarian cancer.

Tumour protein p53‐inducible nuclear protein 1 ( TP 53 INP 1) is a tumour suppressor associated with malignant tumour metastasis. Vasculogenic mimicry ( VM ) is a new tumour vascular supply pattern that significantly influences tumour metastasis and contributes to a poor prognosis. However, the molecular mechanism of the relationship between TP 53 INP 1 and breast cancer VM formation is unknown. Here, we explored the underlying mechanism by which TP 53 INP 1 regulates VM formation in vitro and in vivo. High TP 53 INP 1 expression was not only negatively correlated with a poor prognosis but also had a negative relationship with VE ‐cadherin, HIF ‐1α and Snail expression. TP 53 INP 1 overexpression inhibited breast cancer invasion, migration, epithelial‐mesenchymal transition ( EMT ) and VM formation; conversely, TP 53 INP 1 down‐regulation promoted these processes in vitro by functional experiments and Western blot analysis. We established a hypoxia model induced by CoCl 2 and assessed the effects of TP 53 INP 1 on hypoxia‐induced EMT and VM formation. In addition, we confirmed that a reactive oxygen species ( ROS )‐mediated signalling pathway participated in TP 53 INP 1‐mediated VM formation. Together, our results show that TP 53 INP 1 inhibits hypoxia‐induced EMT and VM formation via the ROS / GSK ‐3β/Snail pathway in breast cancer, which offers new insights into breast cancer clinical therapy.