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首页> 美国卫生研究院文献>Integrative Cancer Therapies >Jianpi-Huayu Formula Inhibits Development of Hepatocellular Carcinoma by Regulating Expression of miR-602 Which Targets the RASSF1A Gene
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Jianpi-Huayu Formula Inhibits Development of Hepatocellular Carcinoma by Regulating Expression of miR-602 Which Targets the RASSF1A Gene

机译：健脾化瘀方通过调节靶向RASSF1A基因的miR-602的表达抑制肝癌的发展。

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摘要

The traditional Chinese medicine formula Jianpi-Huayu (JPHY) has been reported to be effective in the treatment of hepatocellular carcinoma (HCC). However, its underlying mechanism remains unclear. In this article, we employed an orthotopic transplantation model in nude mice to explore whether JPHY could inhibit the development of HCC by regulating miR-602, which targets the Ras association domain-containing protein 1A (RASSF1A) pathway. HCC SMMC-7721 cells were treated with JPHY to test whether the gene as mediated by miR-602 affected the proliferation and apoptosis of tumor cells. We subsequently detected miR-602, RASSF1A, and tumor cell apoptosis–related markers in cells and liver tumor tissues. We observed that mice treated with JPHY had smaller tumors and higher survival rates than untreated ones. Similarly, JPHY-treated SMMC-7721 cells exhibited alterations in morphology and higher cytotoxicity compared with the control group. Furthermore, we found that JPHY decreased overexpression of miR-602 and increased protein expression levels of the gene, which in turn altered protein expression levels of tumor cell apoptosis–related genes in the cells and liver tumor tissues of drug-treated mice. These results indicated that JPHY could potentially be used to treat HCC by targeting miR-602, which targets the gene, which in turn plays a major role in HCC pathogenesis.
机译：据报道，中药配方健脾化瘀（JPHY）可有效治疗肝细胞癌（HCC）。但是，其潜在机制仍不清楚。在本文中，我们采用裸鼠原位移植模型来研究JPHY是否可以通过调节miR-602来抑制HCC的发展，而miR-602的目标是包含Ras缔合域的蛋白1A（RASSF1A）途径。用JPHY处理HCC SMMC-7721细胞，以测试miR-602介导的基因是否影响肿瘤细胞的增殖和凋亡。随后，我们在细胞和肝肿瘤组织中检测到miR-602，RASSF1A和肿瘤细胞凋亡相关标记。我们观察到，用JPHY治疗的小鼠比未治疗的小鼠具有更小的肿瘤和更高的存活率。同样，与对照组相比，经JPHY处理的SMMC-7721细胞表现出形态学改变和更高的细胞毒性。此外，我们发现JPHY减少了miR-602的过表达并增加了该基因的蛋白质表达水平，进而改变了药物治疗小鼠细胞和肝肿瘤组织中与肿瘤细胞凋亡相关基因的蛋白质表达水平。这些结果表明，JPHY可以通过靶向靶向基因的miR-602潜在地用于治疗HCC，而后者又在HCC发病机理中起重要作用。

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