Abstract | OBJECTIVE: METHODS: MG63 and HOS cells were treated with 0.1, 0.25, and 0.5 mmol/L GA-A, and the changes in cell proliferation, apoptosis and migration were evaluated using MTT assay, flow cytometry, and Transwell assay, respectively. The expressions of STAT3, p38, and NF-κB1 in the cells were analyzed by Western blotting. RESULTS: GA-A effectively inhibited the proliferation of human osteosarcoma HOS and MG-63 cells in a dose-dependent manner, and induced obvious cell apoptosis in both cells. Treatment with 0.5 mmol/L GA-A also resulted in significant inhibition of the invasion of both cells. The results of Western blotting showed that GA-A down-regulated the expression level of phosphorylated STAT3 and increased the phosphorylation level of p38 and NF-κB1 expression in both cells. CONCLUSION: GA-A can induce proliferation inhibition, apoptosis and suppression of invasion in human osteosarcoma HOS and MG-63 cells.
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Authors | Jianli Shao, Zhizhong Li, Genlong Jiao, Guodong Sun, Zhigang Zhou |
Journal | Nan fang yi ke da xue xue bao = Journal of Southern Medical University
(Nan Fang Yi Ke Da Xue Xue Bao)
Vol. 35
Issue 5
Pg. 619-24
(May 2015)
ISSN: 2663-0842 [Electronic] China |
PMID | 26018252
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Heptanoic Acids
- NF-kappa B p50 Subunit
- NFKB1 protein, human
- STAT3 Transcription Factor
- STAT3 protein, human
- Lanosterol
- ganoderic acid A
- p38 Mitogen-Activated Protein Kinases
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Topics |
- Apoptosis
(drug effects)
- Bone Neoplasms
(pathology)
- Cell Line, Tumor
(drug effects)
- Cell Movement
(drug effects)
- Cell Proliferation
(drug effects)
- Heptanoic Acids
(pharmacology)
- Humans
- Lanosterol
(analogs & derivatives, pharmacology)
- NF-kappa B p50 Subunit
(metabolism)
- Osteosarcoma
(pathology)
- Phosphorylation
- STAT3 Transcription Factor
(metabolism)
- p38 Mitogen-Activated Protein Kinases
(metabolism)
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