Prx II is FoxM1-dependently-expressed antioxidant in HCC and function as an enhancer of Ras(G12V) oncogenic potential in hepatic tumorigenesis through activation of ERK/FoxM1/cyclin D1 cascade.
The levels of prx1 transcript were higher than those of prx2 in NSCLC cell lines, and the upstream regulatory sequences of the two genes display striking differences.
In addition, two-dimensional gel electrophoresis and mass spectrometry analysis revealed that Prx2 exists in a more oxidized state in AD brains than in control brains.
Moreover, while up-regulation of Prx II appears to provide evidence for the existence of compensatory response in increased cell loss, up-regulation of Prx VI may be used to discriminate PD from AD as well as DS.
Mild thermotolerance (40 °C) and hyperthermia (42-43 °C) caused increased expression of the antioxidants peroxiredoxin-3 (Prx3) and Prx2, and its hyperoxidized form Prx-SO<sub>3</sub>.
In vivo, the volume and weight of transplanted tumor and the number of liver metastases in the PRRX2 shRNA group were significantly reduced, with the similar protein expression patterns as in vitro.
Plasma levels of Prx2 and Prx5 were remarkably increased in ASD compared to healthy controls, while no significant differences were found in red cell Prx levels.
The level of transcripts and the protein content of Prx1 were increased in reticulocyte and RBCs of BTI patients and the protein content was also found to be higher when compared to beta thalassemia major (BTM), suggesting that this peroxidase could cooperate with Prx2 in the removal of H2O2.
There was a significant association between the expression level of Prx II and various factors, including tumor size, histological differentiation, the depth of invasion, the stage of tumor-node-metastasis (TNM) and lymph node metastasis in GC (P<0.05).
There was a significant association between the expression level of Prx II and various factors, including tumor size, histological differentiation, the depth of invasion, the stage of tumor-node-metastasis (TNM) and lymph node metastasis in GC (P<0.05).
There was a significant association between the expression level of Prx II and various factors, including tumor size, histological differentiation, the depth of invasion, the stage of tumor-node-metastasis (TNM) and lymph node metastasis in GC (P<0.05).
Our study demonstrated that miR-212-5p inhibits TNBC from acquiring the EMT phenotype by downregulating Prrx2, thereby inhibiting cell migration and invasion during cancer progression.
Our study demonstrated that miR-212-5p inhibits TNBC from acquiring the EMT phenotype by downregulating Prrx2, thereby inhibiting cell migration and invasion during cancer progression.
Finally, the significant correlation of PRRX2 expression with poor survival in 118 primary breast tumour samples (P = 0.027) and the increased PRRX2 expression in metaplastic breast carcinoma samples, which is pathogenetically related to EMT, validated the biological importance of PRRX2-enhanced migration and invasion and PRRX2-induced EMT.
Prx II is FoxM1-dependently-expressed antioxidant in HCC and function as an enhancer of Ras(G12V) oncogenic potential in hepatic tumorigenesis through activation of ERK/FoxM1/cyclin D1 cascade.