scholarly journals PRDX2 promotes the proliferation of colorectal cancer cells by increasing the ubiquitinated degradation of p53

2021 ◽  
Vol 12 (6) ◽  
Author(s):  
Wuyi Wang ◽  
Jinlai Wei ◽  
Hairong Zhang ◽  
Xiangru Zheng ◽  
He Zhou ◽  
...  

AbstractColorectal cancer is the most common gastrointestinal cancer and causes severe damage to human health. PRDX2 is a member of the peroxiredoxin family reported to have a high level of expression in colorectal cancer. However, the mechanisms by which PRDX2 promotes the proliferation of colorectal cancer are still unclear. Here, the results indicated that PRDX2 expression was upregulated in colorectal cancer and closely correlated with poor prognosis. Functionally, PRDX2 promoted the proliferation of colorectal cancer cells. Mechanistically, PRDX2 could bind RPL4, reducing the interaction between RPL4 and MDM2. These findings demonstrate that the oncogenic property of PRDX2 may be attributed to its regulation of the RPL4-MDM2-p53 pathway, leading to p53 ubiquitinated degradation.

2018 ◽  
Vol 49 (5) ◽  
pp. 2035-2046 ◽  
Author(s):  
Zhi Chen ◽  
Ruizhi Hou ◽  
Shuohui Gao ◽  
Defeng Song ◽  
Ye Feng

Background/Aims: The present study was aimed at examining Ezrin expression in human colorectal cancer (CRC) tissues and elucidating the influence of baicalein on the proliferation of HCT116 cells. Methods: The expression of Ezrin was determined by qRT-PCR and immunohistochemistry. HCT116 cells were divided into four groups- baicalein groups with various concentrations, pcDNA3.1-Ezrin group, si-Ezrin group and dual inhibitory group (baicalein + si-Ezrin). CCK-8 assay and flow cytometry (FCM) were employed to assess cell proliferation and to detect the distribution of cell cycle respectively. The expression levels of Ezrin protein and cell cycle-associated proteins were detected by using western blot. The proliferation ability of CRC cells was also evaluated in vivo. Results: Ezrin expression in CRC tissues was observably higher than that in adjacent colorectal tissues. With drug concentration and action time of baicalein increasing, the cell propagation capacity of HCT116 cells was decreased and the cell cycle progression was arrested. Ezrin expression was inhibited by the administration of baicalein in a dose-dependent way. The levels of CyclinD1 and CDK4 were also significantly decreased, but the expression of P53 pathway proteins P53 and P21 was markedly upregulated. Conclusion: Baicalein repressed proliferation of human colorectal cancer cells HCT116 and blocked cell cycle through downregulating Ezrin and upregulating P53 pathway-related proteins.


2016 ◽  
Vol 143 (3) ◽  
pp. 419-431 ◽  
Author(s):  
Jing Yao ◽  
Ai Huang ◽  
Xiumei Zheng ◽  
Tao Liu ◽  
Zhenyu Lin ◽  
...  

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