MICAL2 Promotes Proliferation and Migration of Glioblastoma Cells Through TGF-β/p-Smad2/EMT-Like Signaling Pathway

Recent studies showed that molecule interacting with CasL2 (MICAL2) could be a novel tumor growth factor, and it is closely associated with tumor growth and invasion. However, the role it plays in glioblastoma (GBM) and its potential mechanisms are currently unknown. Our study is designed to identif...

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Main Authors: Bei Pu, Xu Zhang, Tengfeng Yan, Yuntao Li, Baohui Liu, Zhihong Jian, Omer Kamal Mahgoub, Lijuan Gu, Xiaoxing Xiong, Ning Zou
Format: Article
Language:English
Published: Frontiers Media S.A. 2021-11-01
Series:Frontiers in Oncology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fonc.2021.735180/full
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author Bei Pu
Xu Zhang
Tengfeng Yan
Yuntao Li
Yuntao Li
Baohui Liu
Zhihong Jian
Omer Kamal Mahgoub
Lijuan Gu
Xiaoxing Xiong
Xiaoxing Xiong
Ning Zou
author_facet Bei Pu
Xu Zhang
Tengfeng Yan
Yuntao Li
Yuntao Li
Baohui Liu
Zhihong Jian
Omer Kamal Mahgoub
Lijuan Gu
Xiaoxing Xiong
Xiaoxing Xiong
Ning Zou
author_sort Bei Pu
collection DOAJ
description Recent studies showed that molecule interacting with CasL2 (MICAL2) could be a novel tumor growth factor, and it is closely associated with tumor growth and invasion. However, the role it plays in glioblastoma (GBM) and its potential mechanisms are currently unknown. Our study is designed to identify the effect of MICAL2 on GBM cells and the potential mechanisms behind it. Here, we found that MICAL2 interacts with TGF receptor-type I (TGFRI) and promotes the proliferation and migration of glioblastoma through the TGF-β/p-Smad2/EMT-like signaling pathway. MICAL2-knockdown inhibited the proliferation of glioblastoma cells, which was related to cell cycle arrest and downregulation of DNA replication. The invasion abilities of U87 and U251 cells were reduced after the knockdown of MICAL2. MICAL2 promoted the growth of GBM in nude mice. High MICAL2 predicts poor outcome of GBM patients. MICAL2 could be identified as a novel promising therapeutic target for human GBM.
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spelling doaj.art-fef30f250ac5468a9d79b53d8dee73f22022-12-21T19:23:36ZengFrontiers Media S.A.Frontiers in Oncology2234-943X2021-11-011110.3389/fonc.2021.735180735180MICAL2 Promotes Proliferation and Migration of Glioblastoma Cells Through TGF-β/p-Smad2/EMT-Like Signaling PathwayBei Pu0Xu Zhang1Tengfeng Yan2Yuntao Li3Yuntao Li4Baohui Liu5Zhihong Jian6Omer Kamal Mahgoub7Lijuan Gu8Xiaoxing Xiong9Xiaoxing Xiong10Ning Zou11Department of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, ChinaDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, ChinaDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, ChinaDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, ChinaDepartment of Neurosurgery, The Affiliated Huzhou Hospital, Zhejiang University School of Medicine (Huzhou Central Hospital), Huzhou, ChinaDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, ChinaDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, ChinaDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, ChinaCentral Laboratory, Renmin Hospital of Wuhan University, Wuhan, ChinaDepartment of Neurosurgery, Renmin Hospital of Wuhan University, Wuhan, ChinaDepartment of Neurosurgery, The Affiliated Huzhou Hospital, Zhejiang University School of Medicine (Huzhou Central Hospital), Huzhou, ChinaDepartment of Radiation Oncology, Hubei Cancer Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaRecent studies showed that molecule interacting with CasL2 (MICAL2) could be a novel tumor growth factor, and it is closely associated with tumor growth and invasion. However, the role it plays in glioblastoma (GBM) and its potential mechanisms are currently unknown. Our study is designed to identify the effect of MICAL2 on GBM cells and the potential mechanisms behind it. Here, we found that MICAL2 interacts with TGF receptor-type I (TGFRI) and promotes the proliferation and migration of glioblastoma through the TGF-β/p-Smad2/EMT-like signaling pathway. MICAL2-knockdown inhibited the proliferation of glioblastoma cells, which was related to cell cycle arrest and downregulation of DNA replication. The invasion abilities of U87 and U251 cells were reduced after the knockdown of MICAL2. MICAL2 promoted the growth of GBM in nude mice. High MICAL2 predicts poor outcome of GBM patients. MICAL2 could be identified as a novel promising therapeutic target for human GBM.https://www.frontiersin.org/articles/10.3389/fonc.2021.735180/fullMICAL2TGF-βEMTproliferationmigration
spellingShingle Bei Pu
Xu Zhang
Tengfeng Yan
Yuntao Li
Yuntao Li
Baohui Liu
Zhihong Jian
Omer Kamal Mahgoub
Lijuan Gu
Xiaoxing Xiong
Xiaoxing Xiong
Ning Zou
MICAL2 Promotes Proliferation and Migration of Glioblastoma Cells Through TGF-β/p-Smad2/EMT-Like Signaling Pathway
Frontiers in Oncology
MICAL2
TGF-β
EMT
proliferation
migration
title MICAL2 Promotes Proliferation and Migration of Glioblastoma Cells Through TGF-β/p-Smad2/EMT-Like Signaling Pathway
title_full MICAL2 Promotes Proliferation and Migration of Glioblastoma Cells Through TGF-β/p-Smad2/EMT-Like Signaling Pathway
title_fullStr MICAL2 Promotes Proliferation and Migration of Glioblastoma Cells Through TGF-β/p-Smad2/EMT-Like Signaling Pathway
title_full_unstemmed MICAL2 Promotes Proliferation and Migration of Glioblastoma Cells Through TGF-β/p-Smad2/EMT-Like Signaling Pathway
title_short MICAL2 Promotes Proliferation and Migration of Glioblastoma Cells Through TGF-β/p-Smad2/EMT-Like Signaling Pathway
title_sort mical2 promotes proliferation and migration of glioblastoma cells through tgf β p smad2 emt like signaling pathway
topic MICAL2
TGF-β
EMT
proliferation
migration
url https://www.frontiersin.org/articles/10.3389/fonc.2021.735180/full
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