This study provides a new insight into the regulation of chemotherapy resistance in bladder cancer by PRDX2. Targeting PRDX2 can serve as a potent therapeutic target for chemotherapy resistance.
Collectively, these results indicate PRDX2 as a direct target of Triptolides for inducing apoptosis. Our results not only provide novel insight into the underlying mechanisms of Triptolide-induced cytotoxic effects, but also indicate PRDX2 as a promising potential therapeutic target for developing anti-gastric cancer agents.
A proper PRDX2 balance is therefore crucial. The imbalance causes a number of illnesses, including cancers, inflammatory diseases, cardiovascular ailments, and neurological and neurodegenerative problems which are discussed in this review.
PRDX2 also was found to activate the Wnt/β-catenin pathway by inducing β-catenin nuclear translocation. Consequently, we proved that silencing PRDX2 could inhibit proliferation and Wnt/β-catenin pathway while promoting senescence in HCC cells.
In conclusion, Exo miR-23a-5p inhibited HCC proliferation and angiogenesis by regulating PRDX2 expression. Our results revealed the role and specific molecular mechanism of exo miR-23a-5p in regulating HCC progression.