ATRA对A549人肺腺癌细胞株增殖、细胞周期的影响及其机制研究

周人杰; 廖卫公; 杨镇洲; 闵家新; 肖颖彬

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ATRA对A549人肺腺癌细胞株增殖、细胞周期的影响及其机制研究

论著 | 更新时间：2026-01-09

- ATRA对A549人肺腺癌细胞株增殖、细胞周期的影响及其机制研究
- Effects and mechanisms of ATRA on proliferation, cell cycle of lung carcinoma cell line A549
- 陆军军医大学学报 2007年29卷第14期页码：1399-1401
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  中图分类号： R329.28;R734.2;R979.12
- 纸质出版：2007
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周人杰,廖卫公,杨镇洲,闵家新,肖颖彬.ATRA对A549人肺腺癌细胞株增殖、细胞周期的影响及其机制研究[J].陆军军医大学学报(原第三军医大学学报),2007,29(14):1399-1401.

　ZHOU Ren-jie,LIAO Wei-gong,YANG Zhen-zhou,MIN Jia-xin,XIAO Ying-bin.Effects and mechanisms of ATRA on proliferation, cell cycle of lung carcinoma cell line A549[J].J Amry Med Univ (J Third Mil Med Univ),2007,29(14):1399-1401.
周人杰,廖卫公,杨镇洲,闵家新,肖颖彬.ATRA对A549人肺腺癌细胞株增殖、细胞周期的影响及其机制研究[J].陆军军医大学学报(原第三军医大学学报),2007,29(14):1399-1401. DOI：

　ZHOU Ren-jie,LIAO Wei-gong,YANG Zhen-zhou,MIN Jia-xin,XIAO Ying-bin.Effects and mechanisms of ATRA on proliferation, cell cycle of lung carcinoma cell line A549[J].J Amry Med Univ (J Third Mil Med Univ),2007,29(14):1399-1401. DOI：

摘要

目的探讨全反式维甲酸（all-trans retinoic acid

ATRA）对A549人肺腺癌细胞株增殖、细胞周期的影响及其可能的分子机制。方法 ATRA处理人肺腺癌细胞株A549，观察A549 细胞生长情况并运用MTT法检测其生长抑制情况，流式细胞仪进行细胞周期分析，Western blot检测CDK4、Rb、p-ERK1/2蛋白的表达，荧光定量PCR法检测CyclinD1 mRNA水平。结果 ATRA具有抑制A549细胞增殖、使细胞周期阻滞于G

期，并下调p-ERK1/2蛋白表达及CyclinD1 mRNA水平的作用。结论 ATRA可能通过下调A549细胞p-ERK1/2蛋白表达及CyclinD1 mRNA水平，使细胞周期阻滞于G

期，从而影响其DNA的合成，抑制其恶性增殖。

Abstract

Objective To investigate the effects and mechanisms of all-trans retinoic acid (ATRA) on the proliferation and cell cycle of lung carcinoma cell line A549. Methods The A549 cells were treated with ATRA at the dosages of 5

50 μmol/ L for 1-7 d. The proliferation of A549 was assessed by MTT method and cell cycle was analyzed by flow cytometry. The expressions of CDK4

Rb and p-ERK1/2 were assessed by Western blotting. CyclinD1 mRNA was analyzed by SYBR-PCR amplification. Results ATRA obviously inhibited the proliferation of A549 cells

and the cell cycle was arrested in G

phase. The expression of p-ERK1/

2 protein and CyclinD1 mRNA on A549 cells were decreased. Conclusion ATRA might inhibit the proliferation of A549 cells through down-regulating p-ERK1/2 protein and CyclinD1 mRNA.

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