期刊
ONCOTARGET
卷 6, 期 23, 页码 19469-19482出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.3625
关键词
curcumin; angiogenesis; VEGF; anemia; extramedullary hematopoiesis
资金
- Chinese National Nature Sciences Foundation [81421091]
- Ministry of Science and Technology [2012CB967004, 2014CB744501]
- Doctoral Station Science Foundation from the Chinese Ministry of Education [20130091130003]
- Jiangsu Provincial Nature Science Foundation [BE2013630]
- Bureau of Science and Technology of Changzhou, Jiangsu, China [CZ20130011, CE20135013, CZ20120004, CM20122003, WF201207]
- Macau University of Science and Technology [1101]
Curcumin, a natural polyphenol compound from the perennial herb Curcuma longa, has been proved to be beneficial for tumor-bearing animals through inhibiting tumor neovasculature formation, but the underlying mechanisms are unclear. Here, we aim to test whether curcumin affects VEGF-VEGFR2 signaling pathway and attenuates defective hematopoiesis induced by VEGF in tumor model. We demonstrated that curcumin inhibited proliferation, migration of HUVEC under VEGF stimulation and caused HUVEC apoptosis, and blocked VEGFR2 activation and its downstream signaling pathways in vitro. Furthermore, in VEGF over-expressing tumor model, curcumin significantly inhibited the tumor growth accelerated by VEGF in a dose-dependent manner and improved anemia and extramedullary hematopoiesis in livers and spleens of tumor-bearing mice induced by tumor-derived VEGF. Immunohistochemical analysis showed that curcumin normalized vasculature structures of livers and reduced tumor microvessel density. ELISA revealed that curcumin suppressed VEGF secretion from tumor cells both in vitro and in vivo. Survival analysis showed that curcumin significantly improved survival ability of VEGF tumor-bearing mice. Taken together, these findings establish curcumin as a modulator of VEGF and VEGF-VEGFR2 signaling pathway, with potential implication for improving the quality of life of cancer patients.
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