期刊
INTERNATIONAL IMMUNOPHARMACOLOGY
卷 65, 期 -, 页码 429-437出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.intimp.2018.10.035
关键词
Cryptotanshinone; Colon cancer; Growth; Inflammation; Tumor angiogenesis; Hypoxia inducible factor-1 alpha
资金
- National Natural Science Foundation of China [81703884, 21801138]
- Natural Science Foundation of the Jiangsu Higher Education Institutions of China [17KJB360012]
- Research Innovation Program for College Graduates of Jiangsu Province [KYCX18_2435]
- Nantong City Science and Technology Project [MS12017021-1, MS12015052]
The aim of this study was to evaluate the pharmacological effects of CPT on CT26 colon cancer cells in vivo and in vitro, and to reveal the potential mechanism. CPT suppressed the proliferation and growth of CT26 colon cancer in vitro and in vivo. CPT inhibited the invasion of CT26 cells in vitro, and decreased the protein expressions of matrix metalloproteinase-2 (MMP-2) and MMP-9 but increased those of tissue inhibitor of metallopeptidase-1 (TIMP-1) and TIMP-2 in vitro and in vivo. It also inhibited tumor cell-induced angiogenesis of endothelial cells in vitro and rat aortic ring angiogenesis ex vivo, and possibly by suppressing angiogenesis-associated factors. CPT suppressed the expressions of inflammatory factors in vivo and in vitro. Mechanism studies showed that CPT inhibited the PI3K/AKT/mTOR signaling pathway, as evidenced by decreased expressions of phospho-PI3K (p-PI3K), p-Akt and p-mTOR. Moreover, CPT significantly suppressed the nuclear expression but increased the cytosolic expression of hypoxia inducible factor-1 alpha (HIF-1 alpha). Collectively, CPT inhibited the growth, invasion, inflammation and angiogenesis in CT26 colon cancer, and at least partly, by regulating the PI3K/Akt/mTOR signaling and the nuclear translocation of HIF-1 alpha.
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