Shang Yu-Kui, Li Fanni, Zhang Yi, Liu Ze-Kun, Wang Zi-Ling, Bian Huijie, Chen Zhi-Nan
College of Life Sciences and Bioengineering, Beijing Jiaotong University, Beijing State Key Laboratory of Cancer Biology, Cell Engineering Research Center & Department of Cell Biology, Fourth Military Medical University, Xi'an, China.
Medicine (Baltimore). 2018 Jun;97(23):e10892. doi: 10.1097/MD.0000000000010892.
The carcinogenesis of hepatocellular carcinoma (HCC) is a complex process, starting from a chronically altered hepatic microenvironment due to liver cirrhosis and ultimately progressing to HCC. However, the sequential molecular alterations driving the malignant transformation in liver cirrhosis are not clearly defined.In this study, we obtained gene expression profiles of HCC, including 268 tumor tissues, 243 adjacent tumor tissues, and 40 cirrhotic tissues (GSE25097) from Gene Expression Omnibus (GEO), to comprehensively define changes in the transcriptome of HCC during the sequential evolution of liver cirrhosis into HCC.We showed that changes in the molecular profiles of cirrhotic and adjacent tumor samples were small and quite uniform, whereas there was a striking increase in the heterogeneity of tumors in HCC tissues at the mRNA level. A massive deregulation of key oncogenic molecules and pathways was observed from cirrhosis to HCC tumors. In addition, we focused on FOXO1 and DCN, 2 critical tumor suppressor genes that play an important role in liver cirrhosis and HCC development. FOXO1 and DCN expression levels were significantly reduced in tumor tissues compared with adjacent tumor tissues in HCC. Kaplan-Meier analysis revealed that FOXO1 and DCN expression was positively correlated with overall survival, defining FOXO1 and DCN as adverse prognostic biomarkers for HCC.This system-level research provided new insights into the molecular mechanisms of HCC carcinogenesis. FOXO1 and DCN may be applied as potential targets for HCC treatment in the future.
肝细胞癌(HCC)的致癌作用是一个复杂的过程,始于由于肝硬化导致的长期改变的肝脏微环境,并最终发展为HCC。然而,驱动肝硬化恶性转化的一系列分子改变尚未明确界定。在本研究中,我们从基因表达综合数据库(GEO)中获得了HCC的基因表达谱,包括268个肿瘤组织、243个肿瘤旁组织和40个肝硬化组织(GSE25097),以全面界定肝硬化向HCC逐步演变过程中HCC转录组的变化。我们发现,肝硬化和肿瘤旁样本的分子谱变化很小且相当一致,而在mRNA水平上,HCC组织中肿瘤的异质性显著增加。从肝硬化到HCC肿瘤,观察到关键致癌分子和信号通路的大量失调。此外,我们聚焦于FOXO1和DCN这两个在肝硬化和HCC发展中起重要作用的关键肿瘤抑制基因。与HCC中的肿瘤旁组织相比,肿瘤组织中FOXO1和DCN的表达水平显著降低。Kaplan-Meier分析显示,FOXO1和DCN表达与总生存期呈正相关,将FOXO1和DCN定义为HCC的不良预后生物标志物。这项系统水平的研究为HCC致癌作用的分子机制提供了新的见解。FOXO1和DCN未来可能作为HCC治疗的潜在靶点。