Peroxiredoxin 5 overexpression enhances tumorigenicity and correlates with poor prognosis in gastric cancer
Peroxiredoxin 5 overexpression enhances tumorigenicity and correlates with poor prognosis in gastric cancer
复制标题
DOI：
10.3892/ijo.2017.4013
复制
发表时间：
2017-07-01
影响因子：
5.2
通讯作者：
Lee, Dong-Seok
中科院分区：
文献类型：
--
作者：
Kim, Bokyung;Kim, Yeon Soo;Lee, Dong-Seok
胃癌是全球癌症相关死亡的主要原因之一。尽管目前有先进的手术切除技术和抗癌药物可用于治疗早期胃癌，但胃癌患者的预后仍然很差。上皮向间充质转化(EMT)是肿瘤发生的重要过程。最近的研究表明，活性氧(ROS)可以促进细胞迁移和侵袭。因此，氧化还原动态平衡的失衡会导致癌细胞表现出EMT特性。PRX在乳腺癌、膀胱癌、肺癌、宫颈癌、卵巢癌、前列腺癌、食道癌和肝细胞癌中表达上调。然而，PRX的表达及其对疾病预后、患者存活率和EMT的影响很少在人类胃癌的背景下进行研究。在胃癌患者中，PRX5的表达与肿瘤大小、肿瘤深度、淋巴侵犯密切相关。此外，PRX5的过表达通过上调Snail的表达增加了胃癌细胞的增殖和侵袭力，从而增强了致癌性。综上所述，我们认为PRX5可能是通过增强间充质表型而导致胃癌预后不良的一个潜在因素。最后，PRX5可能是治疗多种过表达PRX5的肿瘤的治疗靶点和临床策略。
Gastric cancer is one of the leading causes of cancer related deaths worldwide. Despite the advanced surgical resection techniques and anticancer drugs currently available to treat early stage gastric cancer, the prognosis of patients with gastric cancer remains poor. The epithelial to mesenchymal transition (EMT) is an important process for the initiation of tumorigenesis. Recent studies suggested that reactive oxygen species (ROS) can promote cell migration and invasion. Thus, an imbalance of redox homeostasis can result in cancer cells exhibiting EMT properties. PRXs are upregulated in various tumors in the breast, bladder, lung, cervical, ovarian, prostate, esophageal, and hepatocellular. However, PRX expression and its impact on disease prognosis, patient survival rate, and EMT are rarely studied in the context of human gastric cancer. The expression of PRX5 was significantly correlated with tumor size, depth of tumor, lymphatic invasion in patients of gastric cancer. In addition, overexpression of PRX5 enhanced carcinogenicity by increasing the proliferation and invasiveness of gastric cancer cells via upregulation of Snail. Taken together, we suggest that PRX5 may be a potential factor that may contribute to poor prognosis of gastric cancer through enhancing the mesenchymal phenotype. Finally, PRX5 is a putative therapeutic target and clinical strategy for various cancers overexpressing PRX5.