Zhang Sheng, Zhang Kang, Ji Piyou, Zheng Xuqing, Jin Jianbin, Feng Min, Liu Pingguo
Department of Hepatobiliary Surgery, ZhongShan Hospital Xiamen University, Xiamen, China.
Fujian Provincial Key Laboratory of Chronic Liver Disease and Hepatocellular Carcinoma (Xiamen University Affiliated ZhongShan Hospital), Xiamen, China.
BMC Cancer. 2017 May 26;17(1):380. doi: 10.1186/s12885-017-3373-7.
Increasing evidence indicates that abnormal expression of GABPA is associated with tumor development and progression. However, the function and clinicopathological significance of GABPA in hepatocellular carcinoma (HCC) remain obscure.
The mRNA and protein expression of GABPA in HCC clinical specimens and cell lines was examined by real-time PCR and western blotting, respectively. Follow-up data were used to uncover the relationship between GABPA expression and the prognosis of HCC patients. HCC cell lines stably overexpressing or silencing GABPA were established to explore the function of GABPA in HCC cell migration and invasion by Transwell and wound healing assays in vitro and in a xenograft model in vivo. Restoration of function analysis was used to examine the underlying molecular mechanisms.
GABPA was downregulated at the protein and mRNA levels in HCC tissues compared with adjacent normal tissues. Decreased GABPA expression was correlated with alpha-fetoprotein levels (P = 0.001), tumor grade (P = 0.017), and distant metastasis (P = 0.021). Kaplan-Meier survival analysis showed that patients with lower GABPA expression had significantly shorter survival times than those with higher GABPA (P = 0.031). In vivo and in vitro assays demonstrated that GABPA negatively regulated HCC cell migration and invasion, and the effect of GABPA on HCC cell migration was mediated at least partly by the regulation of E-cadherin.
Collectively, our data indicate that GABPA inhibits HCC cell migration by modulating E-cadherin and could serve as a novel biomarker for HCC prognosis. GABPA may act as a tumor suppressor during HCC progression and metastasis, and is a potential therapeutic target in HCC.
越来越多的证据表明,GABPA的异常表达与肿瘤的发生和发展有关。然而,GABPA在肝细胞癌(HCC)中的功能及临床病理意义仍不清楚。
分别采用实时PCR和蛋白质免疫印迹法检测HCC临床标本和细胞系中GABPA的mRNA和蛋白表达。利用随访数据揭示GABPA表达与HCC患者预后之间的关系。通过体外Transwell和伤口愈合试验以及体内异种移植模型,建立稳定过表达或沉默GABPA的HCC细胞系,以探讨GABPA在HCC细胞迁移和侵袭中的作用。采用功能恢复分析来研究潜在的分子机制。
与癌旁正常组织相比,HCC组织中GABPA的蛋白和mRNA水平下调。GABPA表达降低与甲胎蛋白水平(P = 0.001)、肿瘤分级(P = 0.017)和远处转移(P = 0.021)相关。Kaplan-Meier生存分析显示,GABPA表达较低的患者生存时间明显短于GABPA表达较高的患者(P = 0.031)。体内和体外试验表明,GABPA负向调节HCC细胞的迁移和侵袭,且GABPA对HCC细胞迁移的影响至少部分是通过调节E-钙黏蛋白介导的。
总体而言,我们的数据表明,GABPA通过调节E-钙黏蛋白抑制HCC细胞迁移,并可作为HCC预后的新型生物标志物。GABPA在HCC进展和转移过程中可能起肿瘤抑制作用,是HCC潜在的治疗靶点。