西妥昔单抗联合紫杉醇对人鼻咽癌CNE-1细胞活力的影响及其可能的分子机制探讨

Effects of Cetuximab Combined with Paclitaxel on Proliferation and Migration of Nasopharyngeal Carcinoma Cell Line CNE-1 and Its Possible Molecular Mechanisms

目的研究西妥昔单抗联合紫杉醇对人鼻咽癌CNE-1细胞活力的影响及其可能分子机制。方法培养人鼻咽癌CNE-1细胞株,分为空白对照组、西妥昔单抗组、紫杉醇组、联合用药组,通过噻唑蓝(MTT)法检测细胞活力、划痕试验检测细胞迁移能力、Western-blot法检测基质金属蛋白酶2(MMP-2)、表皮生长因子受体(EGFR)的mRNA和蛋白水平。结果 1联合用药组的MTT值(36±7)和迁移能力相对值(21±6),低于西妥昔单组的MTT值(62±10)、迁移能力相对值(55±10)和紫杉醇组的MTT值(59±11)、迁移能力相对值(57±10),差异有统计学意义(P<0.05)。2联合用药组EFGR、MMP-2的mRNA含量分别为(50±14)、(45±11),低于西妥昔单组的(67±18)、(69±16)和紫杉醇组的(60±17)、(64±19),差异均有统计学意义(P<0.05);联合用药组的EFGR、MMP-2蛋白含量分别为(43±13)、(36±8),低于西妥昔单组的(69±15)、(64±10)和紫杉醇组(56±14)、(63±9),差异均有统计学意义(均P<0.05)。结论西妥昔单抗联合紫杉醇能够抑制人鼻咽癌CNE-1细胞的增殖和迁移能力,这一作用可能是通过抑制EFGR、MMP-2的表达来实现的。

Objective To study the effect of cetuximab combined with paclitaxel on proliferation and migration of nasopharyngeal carcinoma cell line CNE-I and its possible molecular mechanism. Methods Nasopharyngeal carcinoma cell line CNE-1 were cultured and divided into blank contrast group, cetuximab group, paclitaxel group and combination group. Then ceil vitality was detected by MTT, migration was detec- ted by wound-healing assay and level of matrix metalloproteinase-2 （ MMP-2）, epithelial growth factor recep- tor （EGFR） was detected by real-time PCR and Western-blot. Results （±）MTT value（36 ± 7 ） and migra- tion ability（21 ±6） of the combination group were lower than MTY value（62 ± 10） and migration ability（55 ± 10） of the cetuximab group, MTY value（59 ± 11 ） and migration ability（57 ± 10 ） of the paclitaxel group （P 〈0.05）. （±）EGFR, MMP-2 mRNA levels （50 ± 14）, （45 ± 11 ） of the combination group were lower than （67 ± 18）, （69 ± 16） of the cetuximab group, （60 ± 17）, （64 ± 19） of the paclitaxel group（P 〈 0.05 ） ;EGFR, MMP-2 protein levels （43 ± 13 ）, （36 ± 8 ） of the combination group were lower than （69 ± 15 ）, （64 ± 10 ） of the cetuximab group and （ 56 ± 14 ）, （ 63 ± 9 ） of the paclitaxel group （ P 〈 0.05 ）. Conclusion Ceumimab combined With paclitaxel can reduce the migration and proliferation ability of carci- noma cell line CNE-1, and inhibition on MMP-2, EGFR might be the molecular mechanisms.