Hou Teng, Zhou Lijie, Wang Longwang, Kazobinka Gallina, Chen Yumao, Zhang Xiaoping, Chen Zhaohui
Department of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Department of Urology, The Second Affiliated Hospital of Nanchang University, Nanchang, China.
Cell Physiol Biochem. 2018;47(6):2250-2260. doi: 10.1159/000491536. Epub 2018 Jul 5.
BACKGROUND/AIMS: Leupaxin (LPXN) is a member of the paxillin protein family. Several studies have reported that LPXN regulates cancer development; however, the role of LPXN in bladder cancer remains unknown.
The expression of LPXN in bladder cancer cells and tissues was determined by real-time PCR, western blotting, and immunohistochemistry, respectively. The biological role of LPXN in bladder cancer cell proliferation, invasion, and angiogenesis was explored both in vitro and in vivo.
LPXN expression was elevated in bladder cancer tissues and cell lines compared to adjacent non-tumor tissues and normal urothelial cells. High LPXN expression was correlated with large tumor size, advanced tumor stage, and poor survival in bladder cancer patients. Overexpression of LPXN significantly promoted the proliferation, invasion, and angiogenesis of bladder cancer cells, while suppressing LPXN had the opposite effects. The impact on tumor progression was abolished by inhibiting PI3K/ AKT signaling pathway. We further demonstrated that LPXN probably up-regulated S100P via the PI3K/AKT pathway.
LPXN may facilitate bladder cancer progression by upregulating the expression of S100P via PI3K/AKT pathway. These results provide a novel insight into the role of LPXN in tumorigenesis and progression of bladder cancer and potential therapeutic target of bladder cancer.
背景/目的：白细胞适配蛋白（LPXN）是桩蛋白家族的成员。多项研究报道LPXN可调节癌症发展；然而，LPXN在膀胱癌中的作用尚不清楚。
分别通过实时聚合酶链反应、蛋白质免疫印迹法和免疫组织化学法检测LPXN在膀胱癌细胞和组织中的表达。在体外和体内探究LPXN在膀胱癌细胞增殖、侵袭及血管生成中的生物学作用。
与相邻非肿瘤组织和正常尿路上皮细胞相比，LPXN在膀胱癌组织和细胞系中的表达升高。LPXN高表达与膀胱癌患者的肿瘤体积大、肿瘤分期晚及生存率低相关。LPXN过表达显著促进膀胱癌细胞的增殖、侵袭及血管生成，而抑制LPXN则产生相反作用。抑制PI3K/AKT信号通路可消除对肿瘤进展的影响。我们进一步证明，LPXN可能通过PI3K/AKT途径上调S100P的表达。
LPXN可能通过PI3K/AKT途径上调S100P的表达促进膀胱癌进展。这些结果为LPXN在膀胱癌发生发展中的作用及膀胱癌潜在治疗靶点提供了新的见解。
