PQ401, an IGF-1R inhibitor, induces apoptosis and inhibits growth, proliferation and migration of glioma cells

Growth factor signalling pathways transduce extra-cellular physiological cues to guide cells to maintain critical cellular functions, including cell proliferation, survival and metabolism. Dysregulation of certain growth factor signalling pathways has been shown as a major route to promote tumourige...

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Bibliographic Details
Published in:Journal of chemotherapy (Florence) 2016-01, Vol.28 (1), p.44-49
Main Authors: Zhou, Xiang, Zhao, Xinli, Li, Xiangsheng, Ping, Guanfang, Pei, Sujuan, Chen, Ming, Wang, Zhongwei, Zhou, Wenke, Jin, Baozhe
Format: Article
Language:English
Subjects:
Aminoquinolines - pharmacology
Animals
Apoptosis - drug effects
Blotting, Western
Brain Neoplasms - drug therapy
Brain Neoplasms - metabolism
Brain Neoplasms - pathology
Cell Movement - drug effects
Cell Proliferation - drug effects
Flow Cytometry
Glioma
Glioma - drug therapy
Glioma - metabolism
Glioma - pathology
Humans
IGF1-R
Immunoenzyme Techniques
Male
Mice
Mice, Inbred NOD
Mice, SCID
Migration
Phenylurea Compounds - pharmacology
PQ401
Proliferation
Receptor, IGF Type 1 - antagonists & inhibitors
Tumor Cells, Cultured
U87MG
Xenograft Model Antitumor Assays
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Summary:Growth factor signalling pathways transduce extra-cellular physiological cues to guide cells to maintain critical cellular functions, including cell proliferation, survival and metabolism. Dysregulation of certain growth factor signalling pathways has been shown as a major route to promote tumourigenesis. Glioma is a type of aggressive malignant tumour with no effective systematic therapy so far. Overexpression or hyperactivation of IGF-1R has been observed to be tightly associated with glioma progression and poor prognosis. Here, we examined the biological effects of a specific IGF-1R inhibitor, PQ401, on suppressing U87MG glioma cell growth and migration. Specifically, we observed that PQ401 not only induced cellular apoptosis in U87MG cells and subsequently reduced cell viability and proliferation but also attenuated cell mobility in vitro. More importantly, through a mouse xenograft model, we observed that administration of PQ401 on mice led to suppression of glioma tumour growth in vivo. In summary, our study suggests that PQ401 may serve as a promising leading drug for treating glioma patients with elevated IGF-1R signalling.
ISSN:1120-009X
1973-9478
DOI:10.1179/1973947815Y.0000000026