Abstract | AIM: The aim of this study was to explore the contribution of different doses of Endostar (endostatin, YH-16) on autophagic death in human hepatocellular carcinoma cells. METHODS: RESULTS: Autophagosomes of HepG2 induced by Endostar were observed at 24 hours after treatment, and the amount of autophagosomes increased along with concentration. Meanwhile, Western blotting showed LC3-II protein, indicating the occurrence of autophagy, was expressed to correlate with the dose of Endostar. Meanwhile, the result of the MTT assay showed that the proliferation of cells was inhibited by Endostar in a dose-dependent manner; when the concentration was as high as 400 microg/mL, the inhibition of cells proliferation was 55.0%. CONCLUSIONS: Taken as a whole, the results demonstrate that Endostar suppressed proliferation and triggered cell death in HepG2 cells by autophagy induction that was dose-dependent. These findings provide mechanistic insight into Endostar action.
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Authors | Gang Wu, Ruiguang Zhang, Jinghua Ren, Yichen Sun |
Journal | Cancer biotherapy & radiopharmaceuticals
(Cancer Biother Radiopharm)
Vol. 23
Issue 6
Pg. 735-40
(Dec 2008)
ISSN: 1557-8852 [Electronic] United States |
PMID | 20443695
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Endostatins
- MAP1LC3A protein, human
- Microtubule-Associated Proteins
- Recombinant Proteins
- endostar protein
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Topics |
- Autophagy
- Blotting, Western
- Carcinoma, Hepatocellular
(metabolism, pathology)
- Cell Line, Tumor
- Cell Proliferation
- Endostatins
(genetics, metabolism)
- Humans
- Immunoenzyme Techniques
- Liver Neoplasms
(metabolism, pathology)
- Microtubule-Associated Proteins
(metabolism)
- Recombinant Proteins
(genetics, metabolism)
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