Zingerone suppresses proliferation, invasion, and migration of hepatocellular carcinoma cells by the inhibition of MTDH-mediated PI3K/Akt pathway.

IF 2.6 4区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Receptors and Signal Transduction Pub Date : 2022-08-01 Epub Date: 2021-10-13 DOI:10.1080/10799893.2021.1988970

Jian Fang, Huifen Zhu, Pengcheng Xu, Renya Jiang

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引用次数: 3

Abstract

Purpose: Previous studies have proved that zingerone was a therapeutic agent for many tumors. Metadherin (MTDH) acts as an oncogene and is involved in tumorigenesis. The purpose of this study was to explore the underlying mechanism of zingerone that regulates MTDH to affect hepatocellular carcinoma (HCC) progression.

Methods: CCK-8 assay was performed to detect HCC cell proliferation. The invasion and migration abilities of HCC cells were evaluated using Transwell assay. The mRNA and protein levels in cells and tissues were measured using qRT-PCR and Western blot assays. Moreover, we established the HCC xenografts nude mice to evaluate the effect of zingerone on tumor growth.

Results: We found that zingerone treatment significantly inhibited HCC cell malignant phenotype and tumor growth. Moreover, MTDH was highly expressed in HCC tissues and cell lines and was positively associated with poor overall survival of patients with HCC. Knockdown of MTDH notably suppressed the proliferation, invasion, and migration capacities of HCC cells. Mechanistically, inhibition of MTDH by zingerone impeded the malignant biological behavior of HCC cells by inactivating the PI3K/Akt pathway.

Conclusion: These results suggested that zingerone served as an effective therapeutic agent in HCC via blocking the MTDH-mediated PI3K/Akt pathway.

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姜酮通过抑制mtdh介导的PI3K/Akt通路抑制肝癌细胞的增殖、侵袭和迁移。

目的:前人的研究已经证明生姜酮是一种治疗多种肿瘤的药物。Metadherin (MTDH)是一种致癌基因，参与肿瘤的发生。本研究旨在探讨姜酮调节MTDH影响肝细胞癌(HCC)进展的潜在机制。方法:采用CCK-8法检测肝癌细胞增殖。采用Transwell法评价肝癌细胞的侵袭和迁移能力。采用qRT-PCR和Western blot检测细胞和组织中mRNA和蛋白水平。此外，我们建立了肝癌异种移植裸鼠，以评估姜酮对肿瘤生长的影响。结果:我们发现生姜酮能显著抑制HCC细胞的恶性表型和肿瘤生长。此外，MTDH在HCC组织和细胞系中高表达，并与HCC患者的总生存率低呈正相关。MTDH的下调明显抑制了HCC细胞的增殖、侵袭和迁移能力。从机制上讲，生姜酮抑制MTDH通过灭活PI3K/Akt通路来抑制HCC细胞的恶性生物学行为。结论:生姜酮通过阻断mtdh介导的PI3K/Akt通路，可作为HCC的有效治疗药物。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Journal of Receptors and Signal Transduction 生物-生化与分子生物学

CiteScore

6.60

自引率

0.00%

发文量

审稿时长

>12 weeks

期刊介绍： Journal of Receptors and Signal Tranduction is included in the following abstracting and indexing services: BIOBASE; Biochemistry and Biophysics Citation Index; Biological Abstracts; BIOSIS Full Coverage Shared; BIOSIS Previews; Biotechnology Abstracts; Current Contents/Life Sciences; Derwent Chimera; Derwent Drug File; EMBASE; EMBIOLOGY; Journal Citation Reports/ Science Edition; PubMed/MedLine; Science Citation Index; SciSearch; SCOPUS; SIIC.