摘要
背景与目的观察丹参酮ⅡA对人肺腺癌细胞(SPC-A-1)的抑制作用及其分子机理。方法体外培养的SPC-A-1细胞经无毒剂量(0.5μg/mL)的丹参酮ⅡA处理5天后,观察细胞形态学、增殖动力学、细胞周期分布、细胞凋亡及肿瘤相关基因表达改变,并以全反式维甲酸及顺铂作为对照。结果SPC-A-1细胞经丹参酮ⅡA处理后,细胞生长明显减慢,集落形成率显著降低。FCM细胞周期分析:S期细胞显著减少,G0/G1期细胞则明显增加,细胞凋亡数量显著增加。细胞p53、p21、Fas、Bax表达水平明显升高,而Bcl-2、CDKN2明显降低。结论丹参酮ⅡA对SPC-A-1细胞增殖具有显著抑制作用,其分子机理可能是通过上调p53、p21、Fas、Bax和下调Bcl-2、CKDN2等基因的表达而抑制DNA的合成,同时启动细胞凋亡程序,促进细胞凋亡。
Background and objective To explore the inhibiting effect and its molecular mechanism of Tanshione on human lung carcinoma cell line. Methods Human lung adenocarcinoma cell line （SPC-A-1） was treated IN VITRO with 0.5 μg/mL Tanshinone ⅡA （Tan ⅡA） for five days, other equal cells were also treated with all transretinoic acid （RA） and DDP respectively as control. Changes in cell morphology, proliferation dynamics cell cycle distribution and tumor related genes expression were detected, meanwhile the apoptotic cells and apoptosis related genes expression were detected, too. Results In Tan ⅡA group, the cell growth and rate of clone formation of SPC-A-1 cells were markedly inhibited, Flow Cytometry demonstrated that S phase cells decreased and G0/G1 phase cells increased observably, many apoptotic cells were observed by light and electron microscope. Expression of p53, p21, Fas, Bax was up-regulated obviously while the Bcl-2 and CDKN2 was down-regulated markedly. Conclusion Tan IIA can inhibit cell growth in SPC-A-1 cell line and its possible molecular mechanism may be inhibiting DNA synthesis by upregulating gene p53, p21 and down-regulating gene CDKN2. On the other hand, inducing cell apoptosis by up-regulating gene p53, Fas, Bax and down-regulating gene Bcl-2 might be the other molecular mechanism in suppressing the growth of SPC-A-1 cells.
出处
《中国肺癌杂志》
CAS
2008年第2期202-205,共4页
Chinese Journal of Lung Cancer
基金
四川省科技厅应用基础研究课题资助(No.07JY029-056-1)~~
关键词
丹参酮ⅡA
肺肿癌
增殖抑制
Tanshinone ⅡA Lung neoplasms Growth inhibition
