Crude Extracts of Solanum lyratum Induced Cytotoxicity and Apoptosis in a Human Colon Adenocarcinoma Cell Line (Colo 205)

• Published in: Anticancer research 2008-03, Vol.28 (2A), p.1045-1054
• Main Authors: HSU, Shu-Chun, LU, Jih-Hung, KUO, Chao-Lin, YANG, Jai-Sing, LIN, Meng-Wei, CHEN, Guang-Wei, SU, Chin-Cheng, LU, Hsu-Fung, CHUNG, Jing-Gung
• Format: Article
• Language: English
• Subjects: Adenocarcinoma - drug therapy; Adenocarcinoma - pathology; Apoptosis - drug effects; Biological and medical sciences; Cell Line, Tumor; Cell Survival - drug effects; Colonic Neoplasms - drug therapy; DNA Fragmentation - drug effects; Dose-Response Relationship, Drug; Drug Evaluation, Preclinical; Gastroenterology. Liver. Pancreas. Abdomen; Humans; Medical sciences; Membrane Potential, Mitochondrial; Plant Extracts - pharmacology; Plant Extracts - therapeutic use; Reactive Oxygen Species; Solanum - chemistry; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus; Tumors
• ISSN: 0250-7005; 1791-7530

The effects of the crude extract of Solanum lyratum (SLE) on human colon cancer colo 205 cells were investigated. The cell viability, morphological changes of the cells, cell cycle arrest, apoptosis, reactive oxygen species (ROS), mitochondrial membrane potential (Δæ m ) and cell cycle- and apoptosis-associated protein levels and gene expressions were examined in colo 205 cells after exposure to various concentrations of SLE for different time periods. The results indicated that SLE decreased the percentage of viable colo 205 cells accompanied by morphological changes. The most effective concentration of SLE was 300 μg/ml (SLE 300) and this concentration was used for further investigations. SLE induced S-phase arrest and apoptosis (sub-G1) in the colo 205 cells and those effects were dose- and time-dependent. DAPI staining and DNA gel electrophoresis confirmed that SLE induced apoptosis in colo 205 cells. Flow cytometric analysis also showed that SLE 300 promoted ROS production and decreased the Δæ m . Western blotting analysis indicated that SLE 300 increased Bax levels and decreased Bcl-2 levels, which caused the loss of Δæ m followed by cytochrome c release and caspase-9 and -3 activation, finally leading to apoptosis. SLE 300 also promoted p53 and p27, but decreased the levels of cyclin B1 thus causing S-phase arrest. The gene expression associated with those proteins was also confirmed by PCR methods. The findings show that SLE might be used as a colon cancer therapeutic agent in the future.