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目的探讨低氧对喉癌细胞表达乙酰肝素酶(heparanase,HPSE)蛋白及其侵袭力的影响。方法将Hep-2细胞分为常氧组和低氧组,分别置于常氧(37℃,5%CO2,20%O2)和低氧(37℃,5%CO2,2%O2)条件下培养6、12、24、36h,采用流式细胞学方法对HPSE蛋白表达进行检测,以荧光指数表示HPSE蛋白表达的相对含量,采用基质凝胶侵袭实验检测各组细胞侵袭力。结果常氧及低氧6、12、24、36h状态下Hep-2细胞HPSE蛋白的相对表达量依次升高,常氧组与低氧6h组HPSE蛋白的相对表达量比较差异有统计学意义(P<0·05),常氧组与低氧12、24、36h组HPSE蛋白的相对表达量比较差异有统计学意义(P值均<0·01),而低氧6、12及24h组间荧光指数比较,HPSE蛋白表达量差异有统计学意义(P<0·05);常氧组侵袭细胞数与低氧6h组比较差异无统计学意义(P>0·05),常氧组侵袭细胞数与低氧12h组比较差异有统计学意义(P<0·05),常氧组侵袭细胞数与低氧24、36h组比较差异有统计学意义(P<0·01),而且随着低氧时间延长,侵袭细胞数逐渐增多,组间比较差异有统计学意义(F=20·01,P<0·01),在低氧6~36h期间,低氧引起的细胞侵袭力的提高呈时间依赖性;低氧时HPSE蛋白表达的变化与细胞侵袭力的变化呈正相关(r=0·8092,P<0·01)。结论低氧可显著提高Hep-2细胞HPSE蛋白的表达及其细胞的侵袭力,其侵袭力的增加可能与HPSE表达水平增高有密切关系。
Objective To investigate the effect of hypoxia on the expression of heparanase (HPSE) protein and its invasiveness in laryngeal carcinoma cells. Methods Hep-2 cells were divided into normoxia group and hypoxia group, respectively, under the conditions of normoxia (37 ℃, 5% CO2, 20% O2) and hypoxia The cells were cultured for 6, 12, 24 and 36 h. The expression of HPSE protein was detected by flow cytometry. The relative content of HPSE protein was expressed by fluorescence index. The invasiveness of cells was detected by matrix gel invasion assay. Results The relative expression levels of HPSE protein in Hep-2 cells were increased in the normoxia and hypoxia groups at 6, 12, 24 and 36 h, and the relative expression of HPSE protein in normoxia and hypoxia 6 h groups was significantly different P <0.05). There was significant difference in the relative expression of HPSE protein between normoxia group and hypoxia group at 12, 24, 36 hours (P <0.01) (P <0.05). The number of invasive cells in normoxia group was not significantly different from that in hypoxia 6h group (P> 0.05), the normoxia group The number of invasive cells was significantly different from that in hypoxia 12h group (P <0.05). The number of invasive cells in normoxia group was significantly lower than that in hypoxia 24,36h group (P <0.01) With the prolongation of hypoxia time, the number of invasive cells gradually increased and the difference between the two groups was statistically significant (F = 20.01, P <0.01). During hypoxia for 6 ~ 36h, the invasiveness of cells by hypoxia (P <0.01). The change of HPSE protein expression in hypoxia was positively correlated with the change of cell invasiveness (r = 0.8092, P <0.01). Conclusions Hypoxia can significantly increase the expression of HPSE protein and the invasiveness of Hep-2 cells. The increased invasiveness may be related to the increased expression of HPSE.