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首页> 外文期刊>Hepatology: Official Journal of the American Association for the Study of Liver Diseases >Clinical Correlation of miR-375 and Alpha-Fetoprotein in Hepatocellular Carcinoma: Comparison in Mice and Humans
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Clinical Correlation of miR-375 and Alpha-Fetoprotein in Hepatocellular Carcinoma: Comparison in Mice and Humans

机译：肝细胞癌中miR-375和甲胎蛋白的临床相关性：小鼠和人类的比较

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Reply: We read with great interest the letter by Ho et al., commenting on our study about the increased expression levels of Yes-associated protein (YAP) in chemically induced mouse hepato-cellular carcinomas (HCCs). These increased expression levels were associated with down-regulation of microRNA-375 (miR-375) expression, which is known to control YAP expression, and with enhanced levels of alpha-fetoprotein (AFP), which, in two independent studies, was found to be a target gene of YAP. Ho et al. in their letter show that in 157 HCC, divided into two groups on the basis of the mean levels of miR-375 expression, serum AFP levels were significantly higher in the group showing less reduction in miR-375 than in the group showing stronger reduction of miR-375. Based on these findings, the authors suggest that AFP expression in HCCs is not solely regulated by the axis of miR-375-YAP-AFP. We totally agree with this conclusion. Indeed, as shown in our article, while an anti-correlation exists between miR-375 and YAP expression, such an inverse relation could not be observed between miR and AFP, and nowhere in the text did we imply that a YAP increase could be the main mechanism responsible for AFP regulation. AFP is a well-known marker of HCC and its increase is considered the result of a loss of differentiation of cancer cells. Thus, it seems clear that the increased levels of AFP cannot be due simply to up-regulation of YAP, but rather to a general change in the several factors regulating this protein. Interestingly, the article that originally described AFP as a target gene of YAP was based on a transgenic mouse model where YAP overexpression was induced in newborn (3-week-old) animals. Thus, it is possible that the increased AFP expression observed in YAP-overexpressing mice could also be due to YAP-dependent alteration of hepatocyte differentiation.
机译：答复：我们非常感兴趣地阅读了Ho等人的来信，评论了我们关于化学诱导小鼠肝细胞癌（HCC）中Yes相关蛋白（YAP）表达水平提高的研究。这些增加的表达水平与已知可控制YAP表达的microRNA-375（miR-375）表达下调以及与甲胎蛋白（AFP）的水平升高有关，两项独立研究发现成为YAP的靶基因。 Ho等。他们的信显示，在157例肝癌中，根据miR-375表达的平均水平分为两组，显示miR-375降低较少的组的血清AFP水平显着高于显示miR-375降低的组的血清AFP水平。 miR-375。基于这些发现，作者建议，肝癌中AFP的表达不仅受miR-375-YAP-AFP的轴调控。我们完全同意这一结论。确实，如我们的文章所示，虽然miR-375与YAP表达之间存在反相关关系，但在miR与AFP之间却无法观察到这种反相关关系，在本文中也没有任何地方暗示YAP增加可能是由于负责法新社监管的主要机制。 AFP是HCC的众所周知的标志物，其增加被认为是癌细胞分化丧失的结果。因此，似乎清楚的是，AFP水平的增加不能仅仅由于YAP的上调，而是由于调节该蛋白的几个因素的普遍变化。有趣的是，最初将AFP描述为YAP的靶基因的文章基于转基因小鼠模型，其中在新生（3周龄）动物中诱导了YAP的过表达。因此，有可能在过表达YAP的小鼠中观察到的AFP表达增加也可能归因于肝细胞分化的YAP依赖性改变。

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