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目的 :探讨 9 顺 维甲酸 ( 9 cis RA)的抗肿瘤机理 ,为临床治疗肺癌提供理论依据。方法 :体外培养肺癌细胞株A2、L78、A4 59,随机分组。实验组加 5μmol/L 9 cisRA ,对照组不加 9 cis RA继续培养 ,4 8h后取出 ,用免疫组化SABC法分别检测两组c erbB 2和Rb的基因表达并进行统计学分析。结果 :①实验组、对照组A2株中P185表达率无明显差异 (P >0 .0 5) ,L78株和A549株P185表达率差异非常显著 (P <0 0 1) ;②A2、A549实验组、对照组Rb未见表达 ,L78实验组Rb表达率 9 8% ,对照组Rb无表达 ,差异显著(P <0 0 1)。结论 :① 9 cis RA通过降低c erbB 2表达 ,促使肺癌细胞株分化 ,抑制肺癌细胞株生长 ;② 9 cis RA增强L78细胞株抑癌基因Rb的表达 ,抑制肺癌细胞株的增殖 ,发挥其抗癌作用 ;③ 9 cis RA抑制原癌基因c erbB 2的同时也激活抑癌基因Rb ,协同发挥抗癌作用 ;④ 9 cis RA处理后L78细胞株中Rb表达增加可能与诱导细胞凋亡有关。
Objective: To investigate the antitumor mechanism of 9 cis RA and provide a theoretical basis for clinical treatment of lung cancer. Methods: Lung cancer cell lines A2, L78, A4 59 were cultured in vitro and randomly divided into groups. The experimental group was treated with 5μmol / L 9 cisRA. The control group was cultured without adding 9 cis RA, and the cells were removed after 48 hours. The gene expression of c erbB 2 and Rb were detected by immunohistochemical SABC method and statistically analyzed. Results: ① There was no significant difference in the expression of P185 between experimental group and control group A2 (P> 0.05), but the difference of P185 between L78 and A549 was significant (P <0.01); ②A2, A549 experimental group , No expression of Rb in the control group, Rb expression rate in the L78 experimental group was 98%, but there was no significant difference in the control group (P <0.01). Conclusion: 9 cis RA can promote the differentiation of lung cancer cell lines by inhibiting the expression of c erbB 2 and inhibiting the growth of lung cancer cell lines. ② 9 cis RA enhances the expression of the tumor suppressor gene Rb in L78 cell lines and inhibits the proliferation of lung cancer cell lines, 9 cis RA can inhibit the oncogene c erbB 2 and activate the anti-oncogene Rb simultaneously, which can play an anti-cancer role. ④ The increase of Rb expression in L78 cell line after 9 cis RA treatment may be related to the induction of apoptosis.