Abstract
Hepatocarcinogenesis is a complex and multistep process that involves the accumulation of genetic and epigenetic alterations in regulatory genes. To understand the development of hepatocellular carcinoma (HCC), current research has utilized improved array technologies. The identification of cancer-related molecules could lead to the development of novel molecular targets for treatment and biomarkers for predicting prognosis. However, prognostic prediction is insufficient when considering only tumor factors, since hepatocarcinogenesis is also greatly influenced by the status of the background liver. Clinical background liver factors, such as the presence of chronic active hepatitis or cirrhosis, are well known as risk factors for developing HCC. In contrast, genetic or epigenetic background liver factors remain unknown, albeit those are important to understand the developing process of HCC. Investigating background liver factors could contribute to the development of carcinogenic markers of HCC and to the prevention of the development of HCC. In the present study, we review the currently identified tumor factors and background liver factors from a molecular biological viewpoint and also introduce our combination array analysis.
Highlights
Background liver factorsUnlike other carcinomas, hepatocellular carcinoma (HCC) frequently recurs in residual liver after curative surgical resection
We review the upregulated molecules in HCC as oncogene candidates and downregulated molecules as tumor-suppressor gene (TSG) candidates
High expression of TTK was significantly correlated with AFP, tumor size, advanced stage, PVTT and distant metastasis, and shortened overall survival and disease-free survival
Summary
Numerous studies have revealed the genetic and epigenetic alterations in HCC tissue. The ongoing development and improvement in array technology have contributed to the steady increase in these findings. The authors reported that CTNND1 plays an important role in regulating the EMT to mesenchymal-epithelial transition (MET) plasticity of HCC cells by interacting with E-cadherin, α-catenin, N-cadherin and vimentin and by enhancing Wnt/β‐catenin signaling These studies demonstrate that CTNND1 functions as a novel tumor oncogene in HCC and may be a potential therapeutic target for HCC management. Further mechanistic studies have revealed that TTK activates the Akt/mTOR pathway Together this shows that TTK contributes to HCC tumorigenesis by promoting cell proliferation and migration, and that TTK may serve as a novel biomarker and a potential target in HCC. Zhou et al [154] reported that miR-1180 promoted the proliferation of HCC cells by repressing TNIP2 expression These studies indicate that miR-1180 may act as a tumor promoter by targeting TNIP2 and resisting apoptosis via activation of the NF-κB signaling pathway
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