Abstract
Background/Aims. Hepatocellular carcinoma (HCC) is the lethal digestive cancer and the second leading cause of cancer death in men worldwide. Wnt7a, a 39Kd secreted glycoprotein composed of 349 amino acids, was reported to be related to various diseases. However, its role in HCC has not been studied yet. In this study, using gene expression data and clinical information obtained from the Oncomine and KMplot database, we acknowledged that WNT7A was underexpressed in HCC cancer tissue compared with normal tissue, and WNT7A underexpression was correlated with the decreased survival rate of HCC patients. The function of Wnt7a in cell viability, apoptosis, and migration was evaluated by biological behavior assay and molecular analysis. The findings revealed that WNT7A overexpression significantly restrained cell viability and migration while enhancing apoptosis. In addition, WNT7A overexpression promoted cell apoptosis by strengthening Caspase-3 activity and inhibited migration by downregulating EMT transcriptional factor Snail. Furthermore, the expression level of SKP2 was significantly downregulating in the WNT7A overexpression group. In conclusion, this study illustrated that overexpression of WNT7A inhibited cell viability and migration, which was likely attributed to the regulation of SKP2/P21.
Highlights
Hepatocellular carcinoma (HCC) is the second leading cause of cancer death in men worldwide [1]
In order to understand the potential role of Wnt7a in hepatocellular carcinoma, we analysed the correlation between WNT7A RNA expression levels and overall survival in HCC
All the overall survival analysis including stage I, stage II, and stage III was based on the 364 hepatocellular carcinoma patients from the KM plot database. e p value in stage I was not practically significant (p > 0.05) but significant in stage II (p 0.0062) and stage III (p 0.047). at meant Wnt7a might be a prognostic tool for hepatocellular carcinoma and more possibly affected the late stage. ese data suggest that Wnt7a plays a protective role in the development of hepatocellular carcinoma
Summary
Hepatocellular carcinoma (HCC) is the second leading cause of cancer death in men worldwide [1]. More than 0.7 million deaths from liver cancer occur per year, mostly because of the lack of early diagnosis and treatment. Despite the improvements of liver cancer treatment such as surgical resection, chemotherapy, and radiotherapy, the 5-year survival rate is dismal (below 20%) [2]. Over 80% of patients were diagnosed at a late stage when the tumor has grown and spread; the local treatment was noneffective [3]. Researches on the molecular mechanisms of hepatocellular carcinoma led clinicians and investigators to concentrate on targeted therapy. Only two targeted therapies, sorafenib (an antiangiogenic agent and MAP kinase inhibitor) and regorafenib (a multikinase inhibitor), could increase overall survival [4, 5]
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