目的观察特异结合唾液酸化LewisX(SLeX)抗原DNA适配子抑制HepG2细胞与E一选择素黏附能力及其体外抑制HepG2细胞浸润转移能力。方法采用黏附实验、Transwell体外侵袭实验,检测该适配子对HepG2细胞与E选择素黏附及对HepG2细胞体外侵袭的影响。结果该DNA适配子可有效抑制HepG2细胞与E-选择素黏附,黏附细胞数随适配子浓度的增加而减少(P〈0.01),20nmol浓度的适配子与单克隆抗体CSLEX-1效果相似;Transwell侵袭实验中,5、10、20nmo]适配子组的侵袭细胞数分别为159.00±3.27、142.00±5.50、115.00±5.07,与对照组(178.00±4.64)比较,差异有统计学意义(P〈0.01)。结论特异结合唾液酸化LewisX抗原DNA适配子町以抑制HepG2细胞与E-选择素黏附,阻断Lewis-selectin途径,抑制HepG2细胞体外侵袭转移。
Objective To study the effect of tbe Sialyl LewisX (SLeX) binding DNA aptamer on adhesion and metastasis of hepatocellular carcinoma ( HCC ) HepG2 cells in vitro, and to select possible anti-adhesion drugs for HCC metastasis. Methods The adhesive potential of HepG2 cells to E-selectin and alterations of the adhesive potential after HepG2 cells were sealed by the SLeX binding DNA aptamer were studied by means of the adhesive test. The effect of DNA aptamer on the metastasis of HepG2 ceils was e- valuated by tumor cell migration invasion assays. Results Most of the interactions between E-selectin and the SLeX on the HepG2 cells are specific and could be inhibited by the SLeX binding DNA aptamer. Cell number on the down-side of transwell membrane was significantly less in cells treated with 5, 10, 20 nmol DNA aptamer than in the control cells ( 159. 00 ±3.27, 142. 00 ±5.50 and 115.00 ±5.07, vs. 178.00 ± 4. 64, P 〈 0. 01 ). Conclusion These results indicate that the SLeX binding DNA aptamer can effectively and significantly inhibit the in vitroadhesion, migration, and invasion of HepG2 cells, and also suggest that the SLeX binding DNA aptamer may have potential as an agent to inhibit cancer growth and metastasis.