Feng Jihong, Fu Zhongxue, Guo Jinbao, Lu Weidong, Wen Kunming, Chen Wangsheng, Wang Hao, Wei Jilai, Zhang Shouru
Department of Gastrointestinal Surgery, The First Affiliated Hospital, Chongqing Medical University, Chongqing 400016, P.R. China.
The Affiliated Hospital, Zunyi Medical College, Zunyi, Guizhou 563003, P.R. China.
Mol Med Rep. 2014 Aug;10(2):867-73. doi: 10.3892/mmr.2014.2316. Epub 2014 Jun 10.
Although human peroxiredoxin 2 (PRDX2) has been implicated in tumor progression (e.g., invasion and metastasis), little is known regarding its role in the epithelial‑mesenchymal transition (EMT) process during tumorigenesis. The present study offers the first evidence, to the best of our knowledge, that the antioxidant enzyme PRDX2 has an important role in regulating the EMT process. It was demonstrated that overexpression of PRDX2 leads to changes in cell morphology in vitro and potent inhibition of the transforming growth factor (TGF)‑β1‑induced EMT and cell migration of colorectal cancer (CRC) cells. Furthermore, PRDX2 regulates the expression of EMT markers, EMT‑related transcription factors and metastasis‑related factors in CRC cells. These results provide new insight into the role of PRDX2 in regulating EMT, cell migration and metastasis of CRC cells. It was concluded that the upregulation of PRDX2 may be correlated with EMT and contributes to the pathogenesis of CRC by inhibiting EMT, cell migration and metastasis. Taken together, these findings suggest that PRDX2 may be a key regulator of invasion and metastasis by inhibiting EMT of CRC cells, and also identifies a therapeutic strategy to effectively decrease the lethality of highly malignant types of CRC.
尽管人类过氧化物还原酶2（PRDX2）与肿瘤进展（如侵袭和转移）有关，但其在肿瘤发生过程中的上皮-间质转化（EMT）过程中的作用却知之甚少。据我们所知，本研究首次提供证据表明，抗氧化酶PRDX2在调节EMT过程中具有重要作用。结果表明，PRDX2的过表达导致体外细胞形态发生变化，并有效抑制转化生长因子（TGF）-β1诱导的结直肠癌（CRC）细胞的EMT和细胞迁移。此外，PRDX2调节CRC细胞中EMT标志物、EMT相关转录因子和转移相关因子的表达。这些结果为PRDX2在调节CRC细胞的EMT、细胞迁移和转移中的作用提供了新的见解。研究得出结论，PRDX2的上调可能与EMT相关，并通过抑制EMT、细胞迁移和转移促进CRC的发病机制。综上所述，这些发现表明PRDX2可能是通过抑制CRC细胞的EMT来调节侵袭和转移的关键调节因子，并且还确定了一种有效降低高度恶性类型CRC致死率的治疗策略。
