已发表论文

接触蛋白 2 的 RNAi 通过下调 AICD,EGFR 和 HES1 来抑制 U87 神经胶质瘤干细胞的增殖

 

Authors Guo Y, Zhang PD, Zhang HT, Zhang P, Xu RX

Received 23 May 2016

Accepted for publication 10 November 2016

Published 13 February 2017 Volume 2017:10 Pages 791—801

DOI https://doi.org/10.2147/OTT.S113390

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Colin Mak

Peer reviewer comments 3

Editor who approved publication: Prof. Dr. Geoffrey Pietersz

Abstract: Glioblastoma is the most common form of malignant brain tumors and has a poor prognosis. Glioma stem cells (GSCs) are thought to be responsible for the aberrant proliferation and invasion. Targeting the signaling pathways that promote proliferation in GSCs is one of the strategies for glioma treatment. In this study, we found increased expression of contactin 2 (CNTN2) and amyloid β precursor protein (APP) in U87-derived GSCs (U87-GSCs). RNA interference (RNAi) for CNTN2  downregulated the expression of APP intracellular domain (AICD), which is the proteolytic product of APP. Treatment with CNTN2  RNAi inhibited the proliferation of U87-GSCs. CNTN2  RNAi decreased the expression of epidermal growth factor receptor and HES1, which are potential targets of AICD. In summary, inhibition of the CNTN2/APP signaling pathway may repress the proliferation in U87-GSCs via downregulating the expression of HES1 and epidermal growth factor receptor. CNTN2/APP/AICD signaling pathway plays an important role in U87 glial tumorigenesis. Further studies are warranted to elucidate the role of these signaling pathways in other sources of GSCs. Depending on their role in proliferation in other sources of GSCs, members of the CNTN2/APP/AICD signaling pathway may provide novel targets for the development of therapy for glioblastomas.
Keywords: contactin 2, CNTN2, transient axonal glycoprotein-1, TAG1, glioma stem cells