Abstract
The Melanoma Antigen Gene (MAGE) family is a large, highly conserved group of proteins which was reported to participate in the progression of multiple cancers in humans. However, the function of distinct MAGE genes in hepatocellular carcinoma (HCC) is largely unclear. In this study, we comprehensively evaluated the expression, clinical significance, genetic alteration, interaction network and functional enrichment of MAGEs in HCC. Our research showed that many MAGE genes were dysregulated in HCC. Among them, MAGEA1, MAGEC2, MAGED1, MAGED2, MAGEF1 and MAGEL2 were significantly associated with clinical stage and differentiation of HCC. MAGED1, MAGED2, MAGEA6, MAGEA12, MAGEA10, MAGEB4, MAGEL2 and MAGEC3 significantly correlated with HCC prognosis. Further functional enrichment analysis suggested the dysregulated MAGEs may play important roles in signal transduction. These results indicate that multiple dysregulated MAGEs might play important roles in the development of HCC and can be exploited as useful biomarkers for diagnosis and treatment in HCC.
Highlights
The Melanoma Antigen Gene (MAGE) family is a large, highly conserved group of proteins that share a common MAGE homology domain
As shown in fig.1A MAGEA1、MAGEA6、MAGEA8、MAGEA12、MAGEB1、MAGEB2、MAGEC1、MAGED1、 MAGED2 and MAGEF1 were significantly up-regulated in hepatocellular carcinoma (HCC) tissues compared with non-tumor tissues
MAGED1、MAGED2 and MAGEF1 were significantly up-regulated in HCC tissues and MAGEL2 was significantly down-regulated in HCC tissues
Summary
The Melanoma Antigen Gene (MAGE) family is a large, highly conserved group of proteins that share a common MAGE homology domain. The function of distinct MAGE genes in hepatocellular carcinoma (HCC) is largely unclear. Primary liver cancer is one of the leading causes of cancer-related death worldwide with high incidence rate (4.7%) and mortality rate (8.2%). Hepatocellular carcinoma (HCC) is the main type of primary liver cancer (comprising 75%-85% of cases)[1]. 750000 new cases are diagnosed with HCC and nearly 500000 deaths annually worldwide[2]. Due to the lack of obvious symptom in early stage and effective early diagnosis methods, only 30–40% of HCC patients can be performed curative resection. The grim situation urges us to further elucidate the potential molecular mechanism underlying the occurrence and development of HCC, identify more efficient biomarkers for early diagnosis, prognosis prediction and find new targets to design more powerful therapeutic methods to improve the prognosis of HCC patients
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