Daidzein derivative daid002 inhibits glioblastoma growth via disrupting the interaction between moesin and CD44

Xin Zhang,Wei Zhou,Xiuting Liu,Jinrong Lu,Jinghui Zhang,Qing Wang,Rong Hu

doi:10.18632/oncotarget.24166

Abstract

Daidzein derivative daid002 inhibits glioblastoma growth via disrupting the interaction between moesin and CD44

Highlights

Glioblastoma multiforme (GBM) is the most common malignant brain tumor in adults, with a median survival time of 12–15 months [1]
Moesin phosphorylation induced by CD44/moesin combination promoted cell migration in glioblastoma and CD44/ moesin/β-catenin signaling served as a potential target to inhibit cell proliferation [12]. β-catenin activation played a crucial role in glioblastoma cell differentiation, while CD44, a hyaluronic acid (HA) receptor, was involved in several physiological processes including cell migration, wound healing, leukocyte homing, tumor cell migration and metastasis, and in the meantime referred as a cell surface marker of the cancer stem cells
To explore the inhibitory effects of daid002 (Figure 1) on cancer cell proliferation in general, we examined the effects of daid002 on lung carcinoma cells (A549), colon cancer cells (HCT116), hepatoma carcinoma cells (HepG-2), gastric carcinoma cells (MKN-28), and glioblastoma cells (U87MG) (Figure 2A)

Summary

Introduction

Glioblastoma multiforme (GBM) is the most common malignant brain tumor in adults, with a median survival time of 12–15 months [1]. The current clinical standard of care includes surgical resection, followed by a combination of radiation and chemotherapy [2,3,4]. These treatments failed to provide significant benefit for GBM patients. Moesin phosphorylation induced by CD44/moesin combination promoted cell migration in glioblastoma and CD44/ moesin/β-catenin signaling served as a potential target to inhibit cell proliferation [12]. Β-catenin activation played a crucial role in glioblastoma cell differentiation, while CD44, a hyaluronic acid (HA) receptor, was involved in several physiological processes including cell migration, wound healing, leukocyte homing, tumor cell migration and metastasis, and in the meantime referred as a cell surface marker of the cancer stem cells. HA-CD44-moesin aggregation induced tumor epithelial-mesenchymal transition and high amounts of HA in gliomas have been associated with poor prognosis in GBM patients [13]

Methods

Results

Conclusion