Xie Ming, Xie Ruiyan, Xie Sen, Wu Yiyi, Wang Wei, Li Xiang, Xu Yuanyu, Liu Bo, Zhou Yu, Wang Tao, Gao Lei, Pan Tiejun
Department of Urology, Central Theater Command General Hospital of The Chinese People's Liberation Army, Wuhan, Hubei, China.
Wuhan Clinical Medical College, The First School of Clinical Medicine, Southern Medical University, Wuhan, Hubei, China.
Cell Biol Int. 2020 Oct;44(10):2094-2106. doi: 10.1002/cbin.11418. Epub 2020 Jul 20.
Prostate cancer (PCa) is one of the most common malignant tumors in the world. Thioredoxin interacting protein (TXNIP) is downregulated in a variety of human tumors and plays an important role in tumor suppression. However, the expression level and biological functions of TXNIP in PCa have not been identified yet. Therefore, this study aims to investigate the expression and biological functions of TXNIP in PCa. We reported that the expression of TXNIP was significantly decreased in PCa and associated with clinicopathological features. Overexpression of TXNIP could significantly inhibited PC-3 cells proliferation, migration, invasion, and glucose uptake. Additionally, overexpression of TXNIP could remarkably block cell cycle in the G0/G1 phase and promoted cell apoptosis. Furthermore, TXNIP expression correlated inversely with GLUT1 expression in PCa. Taken together, our results for the first time revealed that TXNIP was decreased in PCa. Moreover, TXNIP might act as a tumor suppressor of PCa and correlated with tumor occurrence and development. Our findings cast a new light on better understanding the occurrence and development of PCa and indicated that TXNIP might be favorable for PCa molecular target therapy.
前列腺癌(PCa)是世界上最常见的恶性肿瘤之一。硫氧还蛋白相互作用蛋白(TXNIP)在多种人类肿瘤中表达下调,并在肿瘤抑制中发挥重要作用。然而,TXNIP在PCa中的表达水平和生物学功能尚未明确。因此,本研究旨在探讨TXNIP在PCa中的表达及生物学功能。我们报道TXNIP在PCa中的表达显著降低,并与临床病理特征相关。TXNIP的过表达可显著抑制PC-3细胞的增殖、迁移、侵袭和葡萄糖摄取。此外,TXNIP的过表达可显著将细胞周期阻滞在G0/G1期并促进细胞凋亡。此外,TXNIP表达与PCa中GLUT1表达呈负相关。综上所述,我们的结果首次揭示TXNIP在PCa中表达降低。此外,TXNIP可能作为PCa的肿瘤抑制因子,并与肿瘤的发生发展相关。我们的发现为更好地理解PCa的发生发展提供了新的线索,并表明TXNIP可能有利于PCa的分子靶向治疗。