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目的探讨细胞视黄酸结合蛋白2(CRABP2)对肺癌细胞应答全反式视黄酸(ATRA)及细胞增殖的影响。方法观察两株肺癌细胞95-D和A549对ATRA的敏感性。应用小干扰RNA(siRNA)敲低CRABP2的表达,采用CCK-8和流式细胞术分别检测细胞增殖和周期变化,Western blot检测NF-κB和丝裂原活化蛋白激酶(MAPKs)信号通路分子的表达。结果 ATRA抑制95-D和A549细胞增殖,其中95-D细胞的抑制作用更为明显;而干扰CRABP2的表达则显著降低ATRA对95-D细胞的抑制作用。干扰CRABP2表达在一定程度上能直接抑制95-D细胞增殖,增加G1期的细胞比例,减少S期的细胞,降低NF-κB、应激活化蛋白激酶/c-JUN氨基末端激酶(SAPK/JNK)和c-JUN的磷酸化水平。结论 CRABP2能增强肺癌细胞对ATRA的敏感性,并且还可能通过调控NF-κB和SAPK/JNK信号通路促进细胞增殖,提示CRABP2在肿瘤细胞中的双重作用。
Objective To investigate the effect of CRABP2 on the expression of all-trans retinoic acid (ATRA) and cell proliferation in lung cancer cells. Methods The sensitivity of ATRA to two lung cancer cell lines 95-D and A549 was observed. The expression of CRABP2 was knocked down with small interfering RNA (siRNA). The cell proliferation and cycle changes were detected by CCK-8 and flow cytometry. The expressions of NF-κB and MAPKs were detected by Western blot expression. Results ATRA inhibited the proliferation of 95-D and A549 cells, and the inhibitory effect of 95-D was more obvious. Interfering with CRABP2 significantly reduced the inhibitory effect of ATRA on 95-D cells. Interfering with CRABP2 expression can directly inhibit the proliferation of 95-D cells to a certain extent, increase the proportion of cells in G1 phase, decrease the number of cells in S phase and decrease the expression of NF-κB, SAPK / cNNK (SAPK / JNK ) And c-JUN phosphorylation levels. Conclusion CRABP2 can enhance the sensitivity of lung cancer cells to ATRA, and may also promote the proliferation of lung cancer cells through the regulation of NF-κB and SAPK / JNK signaling pathways, suggesting that CRABP2 plays a dual role in tumor cells.