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首页> 外文期刊>Cell death and differentiation >LINC00662 promotes hepatocellular carcinoma progression via altering genomic methylation profiles
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LINC00662 promotes hepatocellular carcinoma progression via altering genomic methylation profiles

机译：LINC00662通过改变基因组甲基化型材来促进肝细胞癌进展

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摘要

The identification of viability-associated long noncoding RNAs (lncRNAs) is a means of uncovering therapeutic approaches for hepatocellular carcinoma (HCC). In addition, aberrant genome-wide hypomethylation has been implicated in HCC initiation and progression. However, the relationship between lncRNA dysregulation and genome-wide hypomethylation in hepatocarcinogenesis has not been fully elucidated. A novel lncRNA named LINC00662 was previously demonstrated to play a role in gastrointestinal cancer. In this study, we demonstrated that this lncRNA was correlated with survival and exhibited oncogenic properties, both in vitro and in vivo. Moreover, we determined that LINC00662 could lead to genome-wide hypomethylation and alter the genomic methylation profile by synchronously reducing the S-adenosylmethionine (SAM) level and enhancing the S-adenosylhomocysteine (SAH) level. Mechanistically, LINC00662 was determined to regulate the key enzymes influencing SAM and SAH levels, namely, methionine adenosyltransferase 1A (MAT1A) and S-adenosylhomocysteine hydrolase (AHCY), by RNA-RNA and RNA-protein interactions. In addition, we demonstrated that some SAM-dependent HCC-promoting genes could be regulated by LINC00662 by altering the methylation status of their promoters via the LINC00662-coupled axes of MAT1A/SAM and AHCY/SAH. Taken together, the results of this this study indicate that LINC00662 could be a potential biomarker for HCC therapy. More importantly, we proposed a new role of lncRNA in regulating genomic methylation to promote oncogene activation.
机译：活力相关的长非致rNA（LNCRNA）的鉴定是揭示肝细胞癌（HCC）治疗方法的方法。此外，异常基因组的低甲基化已涉及HCC引发和进展。然而，肝癌发生中的LNCRNA失调和基因组 - 宽的低甲基化之间的关系尚未得到完全阐明。先前证明了一个名为LINC00662的新型LNCRNA在胃肠癌中发挥作用。在这项研究中，我们证明，该LNCRNA与存活率相关，并在体外和体内表现出致癌性质。此外，我们确定LINC00662可以通过同步降低S-腺苷甲基硫氨氨酸（SAM）水平并增强S-腺苷基质细胞（SAH）水平来导致基因组的低甲基化并改变基因组甲基化谱。通过RNA-RNA和RNA-蛋白相互作用，测定LINC00662调节影响SAM和SAH转移酶1A（MAT1A）和S-腺苷基肌细胞水解酶（AHCY）的关键酶。此外，我们证明了LINC00662可以通过通过MAT1A / SAM和AHCY / SAH的LINC00662耦合轴改变其启动子的甲基化状态来调节一些SAM依赖性HCC促进基因。占据了这项研究的结果表明，LINC00662可能是HCC治疗的潜在生物标志物。更重要的是，我们提出了LNCRNA在调节基因组甲基化以促进癌基因活化的新作用。

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