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

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

机构信息

Department of Hepatobiliary Surgery, The Quzhou Affiliated Hospital of Wenzhou Medical University, Quzhou People's Hospital, Quzhou, China.

出版信息

J Recept Signal Transduct Res. 2022 Aug;42(4):409-417. doi: 10.1080/10799893.2021.1988970. Epub 2021 Oct 13.

DOI:10.1080/10799893.2021.1988970
PMID:34645355
Abstract

PURPOSE

Previous studies have proved that zingerone was a therapeutic agent for many tumors. Metadherin () acts as an oncogene and is involved in tumorigenesis. The purpose of this study was to explore the underlying mechanism of zingerone that regulates 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, was highly expressed in HCC tissues and cell lines and was positively associated with poor overall survival of patients with HCC. Knockdown of notably suppressed the proliferation, invasion, and migration capacities of HCC cells. Mechanistically, inhibition of 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 -mediated PI3K/Akt pathway.

摘要

目的

先前的研究已经证明,姜酮是许多肿瘤的治疗剂。Metadherin()作为一种癌基因,参与肿瘤的发生。本研究旨在探讨姜酮调节的潜在机制,以影响肝细胞癌(HCC)的进展。

方法

用 CCK-8 法检测 HCC 细胞的增殖。用 Transwell 测定 HCC 细胞的侵袭和迁移能力。用 qRT-PCR 和 Western blot 法测定细胞和组织中的 mRNA 和蛋白水平。此外,我们建立了 HCC 异种移植裸鼠模型,以评估姜酮对肿瘤生长的影响。

结果

我们发现姜酮处理显著抑制 HCC 细胞的恶性表型和肿瘤生长。此外,在 HCC 组织和细胞系中高度表达,与 HCC 患者的总体生存不良呈正相关。敲低显着抑制了 HCC 细胞的增殖、侵袭和迁移能力。机制上,姜酮通过抑制 PI3K/Akt 通路抑制了 对 HCC 细胞恶性生物学行为的作用。

结论

这些结果表明,姜酮通过阻断-Mediated PI3K/Akt 通路在 HCC 中作为一种有效的治疗剂发挥作用。

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