BACKGROUND: To study the growth-inhibiting effect and its molecular mechanism of Tanshinone on human lung carcinoma cell line. METHODS: Human lung adenocarcinoma cell line (SPC-A-1) was treated in vitro with 0.5μg/ml Tanshinone IIA for five days, and the cells treated with all trans retinoic acid (RA) and DDP as control. Changes in cell morphology, proliferation dynamics, cell cycle distribution and tumor-related gene expression were detected. RESULTS: The cell growth and rate of clone formation of SPC-A-1 cells were markedly inhibited in Tanshinone group than RA group. Flow cytometry demonstrated that S phase cells decreased and G₀/G₁ phase cells increased in Tanshinone group. Expression of p53, p21 was up-regulated obviously but CDKN₂ was down-regulated markedly by Tanshinone IIA. CONCLUSIONS: Tanshinone IIA can inhibit cell growth and clone formation in human lung cancer cell line (SPC-A-1) and its possible molecular mechanism may be inhibiting DNA synthesis by up-regulating p53, p21 and down-regulating CDKN₂.
BACKGROUND: To study the growth-inhibiting effect and its molecular mechanism of Tanshinone on humanlung carcinoma cell line. METHODS:Humanlung adenocarcinoma cell line (SPC-A-1) was treated in vitro with 0.5μg/ml Tanshinone IIA for five days, and the cells treated with all trans retinoic acid (RA) and DDP as control. Changes in cell morphology, proliferation dynamics, cell cycle distribution and tumor-related gene expression were detected. RESULTS: The cell growth and rate of clone formation of SPC-A-1 cells were markedly inhibited in Tanshinone group than RA group. Flow cytometry demonstrated that S phase cells decreased and G₀/G₁ phase cells increased in Tanshinone group. Expression of p53, p21 was up-regulated obviously but CDKN₂ was down-regulated markedly by Tanshinone IIA. CONCLUSIONS:Tanshinone IIA can inhibit cell growth and clone formation in humanlung cancer cell line (SPC-A-1) and its possible molecular mechanism may be inhibiting DNA synthesis by up-regulating p53, p21 and down-regulating CDKN₂.