Erianin suppresses hepatocellular carcinoma cells through down-regulation of PI3K/AKT, p38 and ERK MAPK signaling pathways.

Liang Yang,Qi Chen,Yue Hu,Guanbao Zhou,Zhenshun Song

doi:10.1042/bsr20193137

Abstract

Background: Hepatocellular carcinoma (HCC) is the dominant pathological type of primary liver cancer and no effective methods are available for its treatment. Erianin is a natural product extracted from Dendrobium, which possesses multiple pharmacological activities, including antioxidative and antitumor activity.Objective: To evaluate the anti-HCC activities of erianin and explore its underlying mechanism.Methods: MTT assay and Crystal Violet staining assay were used to select the non-toxic concentrations for the subsequent experiments. The colony formation assay and PCNA fluorescent staining were used to investigate the antiproliferative effects of erianin on human SMMC-7721 and HepG2 cells. Wound healing and transwell test were used to analyze cell migration and invasion. Caspase3 and Tunel staining were used to detect apoptosis. Western blot was used to examine the expression levels of proteins associated with invasion and key proteins in the phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt), p38 and ERK mitogen-activated protein kinase (MAPK) signaling pathways.Results: Erianin inhibited HCC cell proliferation in a dose-dependent manner. Decreased migration rate and invaded cells were observed with erianin supplement. The expression of invasion-associated proteins in the erianin group was also down-regulated. Besides, more apoptotic cells were observed after erianin treatment. For the molecular mechanism, erianin inhibited the phosphorylation of Akt, ERK and P38 in the PI3K/Akt and ERK/P38 pathway.Conclusion: We demonstrated, for the first time, that erianin inhibited the proliferation, migration, invasion and induced the apoptosis of HCC through PI3K/Akt, p38 and ERK MAPK signaling pathway, indicating that erianin is a promising agent for the HCC treatment.

Highlights

Hepatocellular carcinoma (HCC), the dominant pathological type of primary liver cancer, is the third-leading cause of cancer deaths worldwide due to its high rate of recurrence and early metastasis [1,2]
Erianin inhibits the proliferation of HCC cells
To explore the role of the PI3K/AKT pathway in the effect of erianin on HCC cells, we investigated the phosphorylation of AKT after erianin administration by Western blot

Summary

Introduction

Hepatocellular carcinoma (HCC), the dominant pathological type of primary liver cancer, is the third-leading cause of cancer deaths worldwide due to its high rate of recurrence and early metastasis [1,2]. Selective blocking of tumor cell signaling pathways and disrupting. Hepatocellular carcinoma (HCC) is the dominant pathological type of primary liver cancer and no effective methods are available for its treatment. Western blot was used to examine the expression levels of proteins associated with invasion and key proteins in the phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt), p38 and ERK mitogen-activated protein kinase (MAPK) signaling pathways. Erianin inhibited the phosphorylation of Akt, ERK and P38 in the PI3K/Akt and ERK/P38 pathway. Conclusion: We demonstrated, for the first time, that erianin inhibited the proliferation, migration, invasion and induced the apoptosis of HCC through PI3K/Akt, p38 and ERK MAPK signaling pathway, indicating that erianin is a promising agent for the HCC treatment

Objectives

Results

Conclusion