F-01A, an antibiotic, inhibits lung cancer cells proliferation.
10.1016/S1875-5364(14)60055-8
- Author:
Jing WANG
1
,
2
;
Xiao-Peng WU
3
;
Xin-Ming SONG
4
;
Chang-Ri HAN
4
;
Zhong CHEN
5
;
Guang-Ying CHEN
6
Author Information
1. Key Laboratory of Tropical Medicinal Plant Chemistry of Ministry of Education, Hainan Normal University, Haikou 571158, China
2. College of Life Sciences, Hainan Normal University, Haikou 571158, China.
3. Institute of Tropical Bioscience and Biotechnology, Chinese Academy of Tropical Agricultural Sciences, Haikou 571101, China.
4. Key Laboratory of Tropical Medicinal Plant Chemistry of Ministry of Education, Hainan Normal University, Haikou 571158, China.
5. College of Life Sciences, Hainan Normal University, Haikou 571158, China. Electronic address: zh.chen@hainnu.edu.cn.
6. Key Laboratory of Tropical Medicinal Plant Chemistry of Ministry of Education, Hainan Normal University, Haikou 571158, China. Electronic address: chgying123@163.com.
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Membrane potential;
Polyether antibiotic;
SPC-A-1 cells
- MeSH:
Anti-Bacterial Agents;
metabolism;
pharmacology;
Apoptosis;
drug effects;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Cell Survival;
drug effects;
Growth Inhibitors;
pharmacology;
Humans;
Lung Neoplasms;
physiopathology;
Membrane Potential, Mitochondrial;
drug effects;
Streptomyces;
chemistry;
metabolism
- From:
Chinese Journal of Natural Medicines (English Ed.)
2014;12(4):284-289
- CountryChina
- Language:English
-
Abstract:
AIM:In an effort to identify novel, small molecules which can affect the proliferation of lung cancer cells, F-01A, a polyether antibiotic isolated from the fermentation broth of Streptomyces was tested.
METHOD:F-01A was tested for its antitumor properties on the lung cancer cell line SPC-A-1, at six doses (0.1, 0.5, 1, 2.5, and 5 μmol·L(-1)), using various cellular assays. Cell viability was measured by the MTT assay, Hochest 33258 was used to study nuclear morphology; DNA ladder and the loss of mitochondrial membrane potential were also evaluated.
RESULTS:F-01A induces apoptosis against SPC-A-1 cells in a dose-dependent manner. The IC50 is 0.65 μmol·L(-1), and the inhibition at 5 μmol·L(-1) is 87.89%. Further, JC-1 staining indicates F-01A could induce the loss of mitochondrial membrane potential, and the DNA fragment is evident.
CONCLUSION:Mechanistic analysis showed that F-01A induced apoptosis of cancer cells probably in the mitochondrial pathway. The antitumor actions of F-01A involve activation of the apoptotic pathway against SPC-A-1 cells, and it may be valuable for further drug development.
