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Secretome analysis of ionizing radiation-induced senescent cancer cells reveals that secreted RKIP plays a critical role in neighboring cell migration

Authors
Han, Na-KyungKim, Bong ChoLee, Hyung ChulLee, Yoon-JinPark, Myung-JinChi, Sung-GilKo, Young-GyuLee, Jae-Seon
Issue Date
9월-2012
Publisher
WILEY-BLACKWELL
Keywords
Biomedicine; Cellular senescence; Ionizing radiation; RKIP; Secretome; Tumor cells
Citation
PROTEOMICS, v.12, no.18, pp.2822 - 2832
Indexed
SCIE
SCOPUS
Journal Title
PROTEOMICS
Volume
12
Number
18
Start Page
2822
End Page
2832
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/107611
DOI
10.1002/pmic.201100419
ISSN
1615-9853
Abstract
Cellular senescence is a physiological program of irreversible growth arrest that is considered to play an important role in tumor suppression. Recent studies demonstrated that senescent cells secrete multiple growth regulatory proteins that could alter the behavior of neighboring cells. In this study, we investigated the effect of secretory proteins from ionizing radiation (IR) induced senescent tumor cells on normal and tumor cells. Conditioned medium (CM) from IR-induced senescent MCF7 cells significantly increased cell proliferation, invasion, migration, and wound healing activity in MCF7 cells and HUVECs. Comparative proteomics analysis revealed 24 differentially secreted protein spots including Raf kinase inhibitor protein (RKIP), a-Enolase, AKAP9, and MARK4, and the findings were confirmed by Western blot analysis of IR-induced senescent cancer cells. We found that RKIP was secreted via the classical pathway, and the transfection of small interfering RNA against RKIP suppressed CM-induced migration in MCF7 cells. Treatment with recombinant human RKIP increased the migratory activity of MCF7 cells. Taken together, our results demonstrate that the senescence-associated secretory protein RKIP could be the principal target to prevent the potential effects of the secretome from IR-induced senescent tumor cells on neighboring cell migration.
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