Abstract：
Aim: To explore the function and underlying mechanism of MUC13 in hepatocellular carcinoma (HCC) oncogenesis. Materials & Methods: Online databases and software were used to perform analyses of expression, methylation and enrichment pathway. Experiments were performed to confirm the results using HCC cells in vitro. Results: MUC13 was upregulated in HCC and liver cancer stem cells (CSCs) and had a positive influence on CSC generation. Further analyses revealed that MUC13 with promoter hypomethylated was regulated by DNA demethylase TET3, which was overexpressed in HCC and liver CSCs. Conclusion: These results strongly suggested that high TET3 expression in liver CSCs may mediate MUC13 upregulation via promoter hypomethylation and thereby contribute to hepatocellular carcinogenesis.
To understand the function and mechanism of MUC13 in hepatocellular carcinogenesis, online databases and software were used to analyze MUC13 expression, promoter methylation and enrichment pathway. Experiments were also performed to further confirm the results in vitro. MUC13 was upregulated in hepatocellular carcinoma (HCC) and had a positive influence on cancer stem cell (CSC) generation. Further analyses revealed that MUC13 with promoter hypomethylated was regulated by DNA demethylase TET3, which was overexpressed in HCC and liver CSCs. Importantly, it was revealed that MUC13 with promoter hypomethylated, was regulated by TET3, which was overexpressed in HCC and liver CSCs. These results strongly suggest that high TET3 expression in liver CSCs may mediate promoter hypomethylation and expression upregulation of MUC13, thereby contributing to hepatocellular carcinogenesis.
To understand the function and mechanism of MUC13 in hepatocellular carcinogenesis, online databases and software were used to analyze MUC13 expression, promoter methylation and enrichment pathway. Experiments were also performed to further confirm the results in vitro. MUC13 was upregulated in hepatocellular carcinoma (HCC) and had a positive influence on cancer stem cell (CSC) generation. Further analyses revealed that MUC13 with promoter hypomethylated was regulated by DNA demethylase TET3, which was overexpressed in HCC and liver CSCs. Importantly, it was revealed that MUC13 with promoter hypomethylated, was regulated by TET3, which was overexpressed in HCC and liver CSCs. These results strongly suggest that high TET3 expression in liver CSCs may mediate promoter hypomethylation and expression upregulation of MUC13, thereby contributing to hepatocellular carcinogenesis.
摘要：
目的:探讨MUC13在肝细胞癌(HCC)发生发展中的作用及机制。材料和方法：使用在线数据库和软件进行表达分析，甲基化和富集途径。在体外使用HCC细胞进行实验以确认结果。结果：MUC13在HCC和肝癌干细胞（CSCs）中上调，对CSC产生积极影响。进一步的分析表明，启动子低甲基化的MUC13受DNA去甲基酶TET3的调节，该酶在HCC和肝CSC中过表达。结论：这些结果强烈表明，肝脏CSCs中TET3的高表达可能通过启动子低甲基化介导MUC13的上调，从而促进肝细胞癌的发生。
了解MUC13在肝细胞癌变中的功能和机制，在线数据库和软件用于分析MUC13表达，启动子甲基化和富集途径。还进行了实验以进一步证实体外结果。MUC13在肝细胞癌（HCC）中上调，对肿瘤干细胞（CSC）产生积极影响。进一步的分析表明，启动子低甲基化的MUC13受DNA去甲基酶TET3的调节，该酶在HCC和肝CSC中过表达。重要的是,据透露，MUC13与启动子低甲基化，由TET3调节，其在HCC和肝CSC中过度表达。这些结果强烈表明，肝脏CSC中TET3的高表达可能介导MUC13的启动子低甲基化和表达上调，从而促进肝细胞癌变。
了解MUC13在肝细胞癌变中的功能和机制，在线数据库和软件用于分析MUC13表达，启动子甲基化和富集途径。还进行了实验以进一步证实体外结果。MUC13在肝细胞癌（HCC）中上调，对肿瘤干细胞（CSC）产生积极影响。进一步的分析表明，启动子低甲基化的MUC13受DNA去甲基酶TET3的调节，该酶在HCC和肝CSC中过表达。重要的是,据透露，MUC13与启动子低甲基化，由TET3调节，其在HCC和肝CSC中过度表达。这些结果强烈表明，肝脏CSC中TET3的高表达可能介导MUC13的启动子低甲基化和表达上调，从而促进肝细胞癌变。
