OBJECTIVE: To determine the anti-proliferative effect of Tanshinone II A (TAT) on leukemia K562 cell line and its mechanism. METHODS: The proliferation of K562 cell line was detected by MTT assay. The morphological changes of the cells were examined with light microscope. The cell apoptosis was detected by flow cytometry. The expressions of BCL-2, BAX and m-TOR signaling pathway were examined by Western blot assay. RESULTS: TAT inhibited the proliferation of K562 cell line, with a value of IC50 (7.75 +/- 2.47) micromol/L after treatment for 96 h. Significant morphological changes were found after incubation of the cells for 24 h. The apoptotic rate accelerated after TAT treatment for 24 h compared with the controls. TAT down-regulated the expression of mTOR signaling pathway and BCL-2 protein, and up-regulated proapoptotic protein BAX. CONCLUSION: TAT can inhibit the proliferation of K562 cells through down-regulating mTOR signaling pathway, inducing apoptosis.
OBJECTIVE: To determine the anti-proliferative effect of Tanshinone II A (TAT) on leukemia K562 cell line and its mechanism. METHODS: The proliferation of K562 cell line was detected by MTT assay. The morphological changes of the cells were examined with light microscope. The cell apoptosis was detected by flow cytometry. The expressions of BCL-2, BAX and m-TOR signaling pathway were examined by Western blot assay. RESULTS: TAT inhibited the proliferation of K562 cell line, with a value of IC50 (7.75 +/- 2.47) micromol/L after treatment for 96 h. Significant morphological changes were found after incubation of the cells for 24 h. The apoptotic rate accelerated after TAT treatment for 24 h compared with the controls. TAT down-regulated the expression of mTOR signaling pathway and BCL-2 protein, and up-regulated proapoptotic protein BAX. CONCLUSION: TAT can inhibit the proliferation of K562 cells through down-regulating mTOR signaling pathway, inducing apoptosis.