Department of Oncology, Fourth People's Hospital of Zibo, Zibo, China.
Eur Rev Med Pharmacol Sci. 2018 Sep;22(17):5471-5480. doi: 10.26355/eurrev_201809_15807.
The aim of this study was to investigate the expression of UPK1B in bladder cancer (BCa), and to further explore the correlation between UPK1B expression and pathological parameters as well as the prognosis of BCa.
Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression of UPK1B in 92 pairs of BCa tissues and adjacent normal tissues. The relationship between UPK1B expression and pathological features as well as the prognosis of BCa patients was further analyzed. For in vitro experiments, the mRNA expression level of UPK1B in BCa cell lines (EJ and T-24) was detected by qRT-PCR. In addition, knockdown of UPK1B in BCa cells was constructed using small interfering RNA. Effects of UPK1B knockdown on biological functions of BCa cells were analyzed by Cell Counting Kit-8 (CCK-8), colony formation assay and transwell assay, respectively. Furthermore, the underlying mechanism of UPK1B in regulating BCa was evaluated by Western blot and qRT-PCR, respectively.
The expression of UPK1B in BCa tissues was remarkably higher than that of adjacent normal tissues (p<0.05). Compared with BCa patients with lower UPK1B expression, those with higher UPK1B expression exhibited higher tumor stage, lymph node metastasis and distant metastasis. In vitro experiments indicated that cell proliferation, invasion and metastasis were remarkably decreased in cells transfected with si-UPK1B when compared with those transfected with negative controls. Western blot showed that the expression of key proteins in the Wnt/β-catenin signaling pathway in cells transfected with si-UPK1B was significantly down-regulated compared with those transfected with negative controls, including β-catenin, c-myc and cyclinD1. In addition, rescue experiments found that UPK1B was regulated by β-catenin.
UPK1B is upregulated in BCa, and is significantly correlated with tumor stage, lymph node metastasis, distant metastasis and poor prognosis of BCa. Moreover, UPK1B promotes the proliferation, invasion and migration of BCa via regulating the Wnt/β-catenin signaling pathway.
本研究旨在探讨 UPK1B 在膀胱癌（BCa）中的表达，并进一步探讨 UPK1B 表达与病理参数及 BCa 预后的相关性。
采用实时定量聚合酶链反应（qRT-PCR）检测 92 对 BCa 组织及其相邻正常组织中 UPK1B 的表达。进一步分析 UPK1B 表达与 BCa 患者病理特征及预后的关系。体外实验采用 qRT-PCR 检测 UPK1B 在 BCa 细胞系（EJ 和 T-24）中的 mRNA 表达水平。此外，采用小干扰 RNA 构建 BCa 细胞中 UPK1B 的敲低。通过细胞计数试剂盒-8（CCK-8）、集落形成实验和 Transwell 实验分别分析 UPK1B 敲低对 BCa 细胞生物学功能的影响。进一步采用 Western blot 和 qRT-PCR 分别评估 UPK1B 在调控 BCa 中的潜在机制。
UPK1B 在 BCa 组织中的表达明显高于相邻正常组织（p<0.05）。与 UPK1B 低表达的 BCa 患者相比，UPK1B 高表达的患者肿瘤分期更高，淋巴结转移和远处转移更多。体外实验表明，与阴性对照组相比，si-UPK1B 转染的细胞增殖、侵袭和转移能力显著降低。Western blot 显示，与阴性对照组相比，si-UPK1B 转染的细胞中 Wnt/β-catenin 信号通路关键蛋白的表达明显下调，包括β-catenin、c-myc 和 cyclinD1。此外，挽救实验发现 UPK1B 受β-catenin 调控。
UPK1B 在 BCa 中上调，与肿瘤分期、淋巴结转移、远处转移和 BCa 预后不良显著相关。此外，UPK1B 通过调节 Wnt/β-catenin 信号通路促进 BCa 的增殖、侵袭和迁移。
