|Table of Contents|

IGF-1R inhibitor OSI-906 increases radiosensitivity in human nasopharyngeal carcinoma cell line SUNE-1

Journal Of Modern Oncology[ISSN:1672-4992/CN:61-1415/R]

Issue:
2017 02
Page:
167-171
Research Field:
Publishing date:

Info

Title:
IGF-1R inhibitor OSI-906 increases radiosensitivity in human nasopharyngeal carcinoma cell line SUNE-1
Author(s):
Zhao Ming1; Wang Zhe1; Wang Fuguang1; Ju Zaishuang1; Liu Qingping2; Zeng Changqian3; Wang Ruoyu1
1.Department of Oncology,Affiliated Zhongshan Hospital of Dalian University,Liaoning Dalian 116001,China；2.School of Life Science and Biotechnology of Dalian University,Liaoning Dalian 116600,China;3.School of Medicine of Dalian University,Liaoning Dalian 116600,China.
Keywords:
nasopharyngeal carcinoma; radiotherapy; IGF-1R; TKI; radiosensitivity
PACS:
R739.63
DOI:
10.3969/j.issn.1672-4992.2017.02.001
Abstract:
Objective:To explore the mechanism of tyrosine kinase inhibitor （TKI） OSI-906 enhance the radiosensitivity in nasopharyngeal carcinoma cell line.Methods：We examined the effect of OSI-906 on cell proliferation.Then,the activation of AKT and ERK1/2 which were downstream of IGF-1R,detected after X-ray irradiation and OSI-906 addition by Western blot.The cellcycle was examined by flow cytometry.The survival fraction of SUNE-1 wasmeasured by clonogenic assay.Finally,γ-H2AX assay was used to demonstrate OSI-906 induced genomic instability in SUNE-1 cells.Results:OSI-906,significantly suppressed SUNE-1 cell proliferation.X-ray radiation can activate IGF-1R/AKT and IGF-1R/ERK signaling pathways,but both IGF-1R/AKT and IGF-1R/ERK signaling pathways were suppressed by OSI-906.OSI-906 induced SUNE-1 cell cycle arrest in G2/M phase.The combination of irradiation and OSI-906 apparently inhibited SUNE-1 survival ratio than irradiation alone.In addition,OSI-906 treatment increased γ-H2AX foci that induced by irradiation.Conclusion:OSI-906,pIGF-1R TKI,inactives the downstream protein pAKT and pMAPK,inhibits the proliferation of cells,changes the cell cycle and induced genome instability that might be the potential mechanism to enhance the radiosensitivity in NPC cells.

References:

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国家自然科学基金资助项目（编号：81501753）
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