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Marmesin-mediated suppression of VEGF/VEGFR and integrin beta 1 expression: Its implication in non-small cell lung cancer cell responses and tumor angiogenesisopen access

Authors
Kim, Jae HyeonKim, Min SuLee, Bo HeeKim, Jin-KyuAhn, Eun KyungKo, Hye-JinCho, Young-RakLee, Sang-JinBae, Gyu-UnKim, Yong KeeOh, Joa SubSeo, Dong-Wan
Issue Date
Jan-2017
Publisher
SPANDIDOS PUBL LTD
Keywords
marmesin; non-small cell lung cancer; VEGFR-2; VEGF; integrin beta 1
Citation
ONCOLOGY REPORTS, v.37, no.1, pp 91 - 97
Pages
7
Journal Title
ONCOLOGY REPORTS
Volume
37
Number
1
Start Page
91
End Page
97
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/8912
DOI
10.3892/or.2016.5245
ISSN
1021-335X
1791-2431
Abstract
In the present study, we investigated the effects and molecular mechanism of marmesin, a natural coumarin compound isolated from Broussonetia kazinoki, on non-small cell lung cancer (NSCLC) cell responses and tumor angiogenesis. Marmesin abrogated mitogen-stimulated proliferation and invasion in both p53 wild-type A549 and p53-deficient H1299 NSCLC cells. These antitumor activities of marmesin were mediated by the inactivation of mitogenic signaling pathways and downregulation of cell signaling-related proteins including vascular endothelial growth factor receptor-2 (VEGFR-2), integrin beta 1, integrin-linked kinase and matrix metalloproteinases-2. Furthermore, marmesin suppressed the expression and secretion of VEGF in both NSCLC cells, leading to inhibition of capillary-like structure formation in human umbilical vein endothelial cells. Collectively, these findings demonstrate the pharmacological roles and molecular targets of marmesin in regulating NSCLC cell responses and tumor angiogenesis.
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