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目的 探讨抑癌基因p16在维A酸 (RA)对肺癌细胞的增殖抑制和分化调控过程中的作用。方法 运用基因转染技术将抑癌基因p16转入人肺癌细胞A5 49中 ,进而以浓度为 5× 10 6mol/L的全反式维A酸 (ATRA)处理转染和未转染p16基因的肺癌A5 49细胞 1～ 4d ,观察A5 49细胞生长 ,流式细胞仪进行细胞周期分析 ,应用免疫组化分析肺组织分化标志物粘蛋白 (MUC1)的变化 ,同时Westernblot观察ATRA对P16蛋白表达的影响。结果 转染p16抑癌基因的A5 49肺癌细胞经ARTA处理后 ,细胞增殖能力明显下降 ,更多的细胞被阻滞于G1/G0 期 ,MUC1的表达下调 ,Westernblot表明经ATRA处理后P16蛋白表达增加。结论 抑癌基因p16能协同RA抑制肺癌A5 49细胞的恶性增殖及诱导其分化
Objective To investigate the role of p16, a tumor suppressor gene, in the inhibition of proliferation and differentiation of lung cancer cells by tretinoin (RA). Methods The p16 gene was transfected into human lung cancer cell line A5 49 by gene transfection technique, and the transfected and untransfected p16 gene was treated with 5×10 6 mol/L all-trans-retinoic acid (ATRA). Lung cancer A5 49 cells were observed for 1 to 4 days. Growth of A549 cells was observed. Cell cycle analysis was performed by flow cytometry. Changes in lung differentiation marker mucin (MUC1) were analyzed by immunohistochemistry. Western blot was used to observe the expression of P16 protein by ATRA. influences. RESULTS: After transfection of p16 tumor suppressor gene in A5 49 lung cancer cells, the proliferative capacity of A5 49 lung cancer cells decreased significantly, more cells were arrested in G1/G0 phase, and the expression of MUC1 was down-regulated. Western blot indicated that P16 protein expression was detected after ATRA treatment. increase. Conclusion The p16 tumor suppressor gene cooperates with RA to inhibit the malignant proliferation and induce differentiation of lung cancer A5 49 cells.