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观察NK4通过拮抗肝细胞生长因子(HGF)诱导不同肿瘤细胞凋亡,研究其生物学作用及分子机制.以足叶乙甙(VP-16)诱导凋亡,分别或经HGF蛋白、NK4蛋白处理5种肿瘤细胞(B细胞淋巴瘤细胞系Raji、人急性粒细胞白血病细胞系HL-60、宫颈癌细胞系HeLa、前列腺癌细胞系PC-3、非小细胞肺癌细胞系A549),采用流式细胞术(FCM)、吖啶橙(AO)染色法、苏木素-伊红(HE)染色法定量观察5种肿瘤细胞的凋亡情况,并进行相关分析.FCM发现,经VP-16处理5种肿瘤细胞凋亡率均显著高于对照组(P<0.001),而HGF+VP-16组凋亡率明显下降(P<0.01),HGF+NK4+VP-16组细胞凋亡率均明显高于HGF+VP-16组(P<0.05).AO染色和HE染色结果也证实,5种肿瘤细胞经VP-16处理后凋亡率均显著增高(P<0.001,P<0.001),而HGF+VP-16组细胞凋亡率均明显低于VP-16组(P<0.001,P<0.01),HGF+NK4+VP-16组细胞凋亡率均明显高于HGF+VP-16组(P<0.001,P<0.05).此外,发现NK4+VP-16组、HGF+NK4+VP-16组、VP-16组等3组间凋亡率无统计学差异(P>0.05).以上结果提示,HGF蛋白可抵抗凋亡诱导剂VP16的作用,明显降低细胞凋亡;NK4通过竞争性抑制HGF从而促进肿瘤细胞的凋亡,具有潜在的肿瘤治疗价值.
To observe the biological function and molecular mechanism of NK4 induced by different antagonistic hepatocyte growth factor (HGF), and to study the biological function and mechanism of NK4 induced by apoptosis.Epithelial cell apoptosis was induced by NK-protein and NK4 protein respectively Five kinds of tumor cells (B cell lymphoma cell line Raji, human acute myeloid leukemia cell line HL-60, cervical cancer cell line HeLa, prostate cancer cell line PC-3 and non-small cell lung cancer cell line A549) (FCM), acridine orange (AO) staining and hematoxylin-eosin (HE) staining were used to quantitatively observe the apoptosis of the five kinds of tumor cells and to analyze the correlation.FCM found that VP-16 treatment of 5 The apoptosis rate of HGF + VP-16 group was significantly lower than that of control group (P <0.001) (P <0.01), and the apoptosis rate of HGF + NK4 + VP-16 group was significantly higher (P <0.001, P <0.001). The results of AO staining and HE staining also showed that the apoptotic rates of all the 5 tumor cells were significantly increased after VP-16 treatment (P <0.001, P <0.001) (P <0.001, P <0.01). The apoptosis rate of HGF + NK4 + VP-16 group was significantly higher than that of HGF + VP-16 group P <0.001, P <0.05) .In addition, NK4 + VP-16 group, HG were found There was no significant difference in the apoptotic rate between the three groups (F + NK4 + VP-16 group and VP-16 group) (P> 0.05). These results suggest that HGF protein can resist the action of apoptosis inducer VP16, NK4 plays a potential role in tumor therapy by competitive inhibition of HGF to promote apoptosis of tumor cells.