Abstract：
OBJECTIVE: Although aberrant expression of peroxidasin-like (PXDNL) has been associated with carcinogenesis, its potential role in the Urothelial Carcinoma of the Bladder (UCB) remains unknown. The present study aimed to explore the role of PXDNL in UCB carcinogenesis and its potential clinical value.
METHODS: Based on The Cancer Genome Atlas (TCGA) data, bioinformatics was used to explore the potential clinical value of PXDNL. Wound healing and Transwell invasion assays were employed for the purpose of assessing the cell motility, while the Western Blotting experiments were utilized for investigating the protein expression pattern of PXDNL in UCB and investigating the Epithelial-to-Mesenchymal Transition (EMT) and Wnt/β-catenin pathways for understanding the probable mechanisms involved.
UNASSIGNED: PXDNL mRNA was overexpressed in UCB tissues and indicated a poor prognosis. High PXDNL mRNA levels were also associated with advanced clinicopathological features and were regarded as independent prognostic factors for UCB. However, PXDNL showed a weak correlation with immune cell infiltration in UCB. In addition, the findings of the study verified that the existing form of the PXDNL protein was 57-kDa and it was upregulated in the UCB cell lines and tissue samples. Furthermore, silencing PXDNL inhibited, while overexpressing PXDNL promoted EMT and motility of UCB cells in vitro. Mechanistic studies showed that PXDNL activated UCB cell motility via the Wnt/β-catenin pathway.
CONCLUSIONS: The results reveal a novel molecular target that could be further explored for developing preventive, predictive, and individualized treatment strategies for UCB.
METHODS: Based on The Cancer Genome Atlas (TCGA) data, bioinformatics was used to explore the potential clinical value of PXDNL. Wound healing and Transwell invasion assays were employed for the purpose of assessing the cell motility, while the Western Blotting experiments were utilized for investigating the protein expression pattern of PXDNL in UCB and investigating the Epithelial-to-Mesenchymal Transition (EMT) and Wnt/β-catenin pathways for understanding the probable mechanisms involved.
UNASSIGNED: PXDNL mRNA was overexpressed in UCB tissues and indicated a poor prognosis. High PXDNL mRNA levels were also associated with advanced clinicopathological features and were regarded as independent prognostic factors for UCB. However, PXDNL showed a weak correlation with immune cell infiltration in UCB. In addition, the findings of the study verified that the existing form of the PXDNL protein was 57-kDa and it was upregulated in the UCB cell lines and tissue samples. Furthermore, silencing PXDNL inhibited, while overexpressing PXDNL promoted EMT and motility of UCB cells in vitro. Mechanistic studies showed that PXDNL activated UCB cell motility via the Wnt/β-catenin pathway.
CONCLUSIONS: The results reveal a novel molecular target that could be further explored for developing preventive, predictive, and individualized treatment strategies for UCB.
摘要：
目的：尽管过氧化物酶样蛋白（PXDNL）的异常表达与癌变有关，其在膀胱尿路上皮癌（UCB）中的潜在作用尚不清楚。本研究旨在探讨PXDNL在UCB癌变过程中的作用及其潜在的临床价值。
方法：基于癌症基因组图谱（TCGA）数据，生物信息学用于探讨PXDNL的潜在临床价值。为了评估细胞运动性，采用了伤口愈合和Transwell侵袭试验。而WesternBlotting实验用于研究UCB中PXDNL的蛋白质表达模式，并研究上皮-间质转化（EMT）和Wnt/β-catenin途径，以了解可能的机制。
未经证实：PXDNLmRNA在UCB组织中过表达，提示预后不良。高PXDNLmRNA水平也与晚期临床病理特征相关，并被视为UCB的独立预后因素。然而,PXDNL与UCB中的免疫细胞浸润显示弱相关性。此外,这项研究的结果证实，PXDNL蛋白的存在形式为57kDa，并且在UCB细胞系和组织样本中被上调。此外，沉默PXDNL被抑制，而过表达PXDNL在体外促进UCB细胞的EMT和运动。机制研究表明，PXDNL通过Wnt/β-catenin途径激活UCB细胞运动。
结论：结果揭示了一种新的分子靶标，可以进一步探索用于开发预防，预测性，和UCB的个体化治疗策略。
方法：基于癌症基因组图谱（TCGA）数据，生物信息学用于探讨PXDNL的潜在临床价值。为了评估细胞运动性，采用了伤口愈合和Transwell侵袭试验。而WesternBlotting实验用于研究UCB中PXDNL的蛋白质表达模式，并研究上皮-间质转化（EMT）和Wnt/β-catenin途径，以了解可能的机制。
未经证实：PXDNLmRNA在UCB组织中过表达，提示预后不良。高PXDNLmRNA水平也与晚期临床病理特征相关，并被视为UCB的独立预后因素。然而,PXDNL与UCB中的免疫细胞浸润显示弱相关性。此外,这项研究的结果证实，PXDNL蛋白的存在形式为57kDa，并且在UCB细胞系和组织样本中被上调。此外，沉默PXDNL被抑制，而过表达PXDNL在体外促进UCB细胞的EMT和运动。机制研究表明，PXDNL通过Wnt/β-catenin途径激活UCB细胞运动。
结论：结果揭示了一种新的分子靶标，可以进一步探索用于开发预防，预测性，和UCB的个体化治疗策略。
