We found that PRDX2 depletion in mice treated with 5-FU resulted in, inhibition of tumor growth, compared with mice treated with 5-FU alone
2017
Knockdown of PRDX2 sensitizes colon cancer cells to 5-FU by suppressing the PI3K/AKT signaling pathway
Key concepts
Scholarcy highlights
- These findings indicate that PRDX2 could be a potential target to address the problem of 5-FU resistance in colon cancer
- We showed that knocking down PRDX2 in vitro facilitates cell death and apoptosis in colon cancer cells treated with c 2017 The Author(s)
- These results demonstrate that the lentivirus-mediated shRNA targetted PRDX2 effectively and knocked down PRDX2 expression in colon cancer cells
- To determine the role of PRDX2 in colon cancer cells treated with 5-FU, we used the Cell Counting Kit-8 assay to detect the survival rate of colon cancer cells that were stably transfected with NC-shRNA-LV and PRDX2-shRNA-LV and treated with 5-FU at different concentrations for 48 h
- We observed a lower survival rate in the shPRDX2 group, compared with the shCont group. These results indicated that knocking down the expression of PRDX2 increased the chemosensitivity of colon cancer cells to 5-FU, in a dose-dependent manner
- We found that PRDX2 and p-AKT were strongly expressed in the cytoplasm of colon cancer cells, and were weakly expressed in normal colon mucosal tissues
- Our results demonstrate that inhibiting PRDX2 expression promotes 5-FU-induced apoptosis in colon cancer cells via the PI3K/AKT signal pathway
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