Ethyl Acetate Fraction from Hedyotis diffusa plus Scutellaria barbata Suppresses Migration of Bone-Metastatic Breast Cancer Cells via OPN-FAK/ERK/NF-κB Axis.

Ting Fang,Dan-Dan Zhang,Ying-Xuan Yan,Qing-Qi Chang,Yue Yang,Ya-Xin Lv

doi:10.1155/2020/3573240

Abstract

Hedyotis diffusa plus Scutellaria barbata is a couplet of medicinal that has been commonly used to treat inflammation-related diseases and various types of tumors. However, the effect of this couplet on tumor cell migration has not been elucidated. With the aid of MCF-7-BOM, a bone-metastatic subline of ER + breast cancer MCF-7, we showed that ethyl acetate fraction extracted at an equal weight ratio of Hedyotis diffusa plus Scutellaria barbata (EA11) inhibited cell migration of MCF-7-BOM in a concentration-dependent manner. To define the underlying molecular mechanism, we revealed that EA11 reduced the expression of osteopontin (OPN) and interfered with the FAK/ERK/NF-κB signaling pathways, which are both critical for breast cancer bone metastasis. This study strongly suggested EA11 may represent a potential therapeutic agent against bone metastasis of breast cancer.

Highlights

Metastasis is a severe threat to the survival of breast cancer patients worldwide [1, 2], and bone metastasis occurs in approximately 65% of advanced breast cancer patients
To determine the effect of EA11 on MCF-7-BOM cell growth, cells were treated with varying concentrations of EA11 for 72 h followed by MTT assay to measure cell growth
By comparing with the untreated cells, we observed that EA11 at 100 μg/ml significantly inhibited the growth of MCF-7-BOM cells (P < 0.05) (Figure 1), indicating that EA11 at concentration

Summary

Introduction

Metastasis is a severe threat to the survival of breast cancer patients worldwide [1, 2], and bone metastasis occurs in approximately 65% of advanced breast cancer patients. Experimental evidence supports the role of OPN in bone metastasis of breast cancer. The activation of the focal adhesion kinase (FAK) pathway was reported as an inevitable event of OPN-induced cell migration [8]. OPN has been found to activate ERK1/2 through its binding to αvβ integrin [9], which in turn promotes breast cancer progression. OPN has been shown to augment cancer cell invasiveness via the NFκB-mediated signaling mechanism [10]. Ese findings suggest that targeting OPN-associated signaling pathways may be a potential therapeutic strategy against bone metastasis of breast cancer [11, 12] OPN has been shown to augment cancer cell invasiveness via the NFκB-mediated signaling mechanism [10]. ese findings suggest that targeting OPN-associated signaling pathways may be a potential therapeutic strategy against bone metastasis of breast cancer [11, 12]

Methods

Results

Conclusion