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| HSD17B4通过调控氧化应激诱导STAT1表达促进肝癌细胞侵袭迁移 |
| HSD17B4 induces STAT1 expression by regulating oxidative stress to promote hepatocellular carcinoma cell invasion and migration |
| 投稿时间：2024-10-16 修订日期：2024-12-29 |
| DOI： |
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| 中文关键词: HCC HSD17B4 侵袭迁移 氧化应激 STAT1 |
| 英文关键词:HCC HSD17B4 Invasion and migration Oxidative stress STAT1 |
| 基金项目: |
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| 摘要点击次数: 41 |
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| 中文摘要: |
| [目的]探讨17β-羟基类固醇脱氢酶4（17β?hydroxysteroid dehydrogenase 4，HSD17B4）在肝细胞癌（Hepatocellular carcinoma，HCC）恶性进展中的作用及其潜在的作用机制。[方法]免疫组织化学（Immunohistochemistry，IHC）实验检测HCC患者癌组织和癌旁组织HSD17B4蛋白的表达水平；将HSD17B4的干扰RNA（siHSD17B4）和过表达质粒（pCMV6-HSD17B4）分别转染至肝癌细胞中，进行HSD17B4敲降和过表达处理；采用细胞划痕实验和Transwell实验检测肝癌细胞的迁移和侵袭能力；通过蛋白免疫印迹（Western blotting, WB）实验检测波形蛋白（Vimentin, VIM）和基质金属蛋白酶9（Matrix metalloproteinase 9, MMP9）等促侵袭迁移蛋白的表达水平；通过WB实验和细胞免疫荧光技术分别检测HSD17B4对信号转导和转录激活因子1（signal transducer and activator of transcription 1, STAT1）表达的影响和对磷酸化STAT1（p-STAT1）核转位的影响；通过荧光探针和比色法分别检测细胞内的活性氧（Reactive oxygen species, ROS）和丙二醛（Malondialdehyde, MDA）以评估HSD17B4对肝癌细胞内氧化应激的影响。[结果] HSD17B4在HCC患者癌组织中的表达量高于癌旁组织（P<0.05）；HSD17B4过表达后，肝癌细胞的迁移和侵袭能力增强（P<0.05），VIM、MMP9以及STAT1的表达水平均升高（P<0.05），细胞内ROS和MDA水平降低（P<0.05）。HSD17B4敲降后则出现相反的结果（P<0.05）。然而，HSD17B4对p-STAT1核转位的影响并不明显。[结论] HSD17B4可能通过制衡细胞内氧化应激水平调控STAT1的表达从而促进HCC细胞侵袭迁移。 |
| 英文摘要: |
| [Purpose] To explore the function of 17β?hydroxysteroid dehydrogenase 4 (HSD17B4) in hepatocellular carcinoma (HCC) malignant progression and the underlying mechanism of that. [Methods] The expression level of HSD17B4 protein in HCC tissues and adjacent tissues was detected by immunohistochemistry (IHC). HCC cells were transfected with HSD17B4 interference RNA (siHSD17B4) and overexpression plasmid (pCMV6-HSD17B4) to make HSD17B4 knockdown and overexpression respectively. Scratch assay and transwell assay were used to detect the migration and invasion abilities of HCC cells. The expression levels of pro-invasion and migration proteins, such as vimentin (VIM) and matrix metalloproteinase 9 (MMP9), were detected by western blotting (WB). WB and cellular immunofluorescence were separately used to analyze the effects of HSD17B4 on the expression level of signal transducer and activator of transcription 1 (STAT1) and the nuclear translocation of phosphorylated STAT1 (p-STAT1). Intracellular reactive oxygen species (ROS) and malondialdehyde (MDA) were separately detected by fluorescence probe technique and colorimetric method to evaluate the effect of HSD17B4 on oxidative stress in HCC cells. [Results] The expression of HSD17B4 protein in HCC tissue was significantly increased compared with that in adjacent tissue (P<0.05). After HSD17B4 overexpression, the migration and invasion abilities of HCC cells were enhanced (P<0.05), the expression levels of VIM, MMP9, and STAT1 proteins were increased (P<0.05), intracellular ROS and MDA levels were decreased (P<0.05). The opposite results were observed after HSD17B4 knockdown (P<0.05). However, the effect of HSD17B4 on the nuclear translocation of p-STAT1 was not evident. [Conclusion] HSD17B4 could induce STAT1 expression by regulating oxidative stress to promote HCC cell invasion and migration. |
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