肝癌组织中PIVKA-Ⅱ水平及维生素K<sub>2</sub>对肝癌细胞中PIVKA-Ⅱ的影响

张毅敏; 王明丽; 单绿虎; 张剑英; 徐笑红; 夏文进

doi:10.16766/j.cnki.issn.1674-4152.2017.05.033

肝癌组织中PIVKA-Ⅱ水平及维生素K₂对肝癌细胞中PIVKA-Ⅱ的影响

doi: 10.16766/j.cnki.issn.1674-4152.2017.05.033

1. 浙江省肿瘤医院检验科, 浙江杭州 310022;
2. 浙江省中山医院

基金项目:

浙江省医药卫生科技计划项目(2014-KYB-043)

详细信息

通讯作者:
徐笑红,E-mail:zjhzxxh@163.com

中图分类号: R735.7;R446.61;R977.26
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- 被引次数: 0
出版历程
- 收稿日期: 2016-12-02
- 网络出版日期: 2022-08-06

PIVKA-Ⅱ levels in HCC tissues and effect of vitamin K₂ on the expression of PIVKA-Ⅱ in HCC cells

Department of Clinical Oncology, Zhejiang Cancer Hospital, Hangzhou, Zhejiang 310022, China

摘要

摘要: 目的观察肝癌组织中维生素K缺乏或拮抗剂-Ⅱ诱导的蛋白质(protein induced by vitamin K absence or antagonist-Ⅱ,PIVKA-Ⅱ)表达情况及维生素K₂(vitamin K₂,VitK₂)对肝癌细胞中PIVKA-Ⅱ的影响,探讨PIVKA-Ⅱ与肝癌的关系及可能机制。方法选择浙江省肿瘤医院、浙江省中山医院2012年1月-2015年12月100对手术切除的原发性肝癌组织及癌旁组织标本,采用ABC免疫组织化学法测定组织中PIVKA-Ⅱ的阳性表达情况,采用化学发光免疫分析法测定标本中PIVKA-Ⅱ水平;将HepG-2细胞和浓度为20 μM的VitK₂共同培养,酶联免疫吸附(ELISA)法测定VitK₂对HepG-2肝癌细胞PIVKA-Ⅱ表达的影响,MTT法测定VitK₂对HepG-2肝癌细胞生长的影响,Transwell法测定VitK₂对HepG-2肝癌细胞侵袭能力的影响。结果肝癌组织中PIVKA-Ⅱ阳性率(74.0%)高于癌旁组织中PIVKA-Ⅱ阳性表达率(25.0%,P<0.05);肝癌组织中PIVKA-Ⅱ水平(3 786.23±143.24) mAU/g高于癌旁组织中PIVKA-Ⅱ水平(167.34±21.54) mAU/g,P<0.05。对照组肝癌细胞PIVKA-Ⅱ水平为(3.43±0.04) ng/(ml·10⁶细胞),VitK₂组肝癌细胞PIVKA-Ⅱ水平为(2.57±0.02) ng/(ml·10⁶细胞),VitK₂组肝癌细胞PIVKA-Ⅱ水平明显低于对照组(P<0.05)。VitK₂与HepG-2肝癌细胞共同培养,第1天、第2天、第3天、第4天、第5天、第6天时VitK₂对HepG-2细胞的抑制率分别为9.2%、16.5%、26.7%、34.8%、41.2%、46.7%。VitK₂与HepG-2肝癌细胞培养24 h后,VitK₂对HepG-2肝癌细胞侵袭的抑制率为37.2%。结论肝癌组织中PIVKA-Ⅱ呈高表达,VitK₂能够降低肝癌细胞中PIVKA-Ⅱ水平、抑制肝癌细胞生长、降低肝癌细胞侵袭能力。
- 肝细胞癌 /
- 维生素K₂ /
- 维生素K缺乏或拮抗剂-Ⅱ诱导的蛋白质
Abstract: Objective To observe the expression of Vitamin K deficiency or antagonist-Ⅱ-induced protein (PIVKA-Ⅱ) in human hepatocellular carcinoma (HCC) and the effect of vitamin K₂ on the expression of PIVKA-Ⅱ in HCC cells,to explore the relationship between PIVKA-Ⅱ and HCC and its possible mechanism. Methods One hundred pairs of primary liver cancer tissue and adjacent tissue samples of surgical resection in Zhejiang Cancer Hospital from January,2012 to December,2015 were selected.The expression of PIVKA-Ⅱ in tissues was determined by ABC immunohistochemical method.The level of PIVKA-Ⅱ in the samples was determined by electrochemiluminescence immunoassay.HepG-2 cells were co-cultured with VitK₂ at concentration of 20 μM.The effect of VitK₂ on the expression of PIVKA-Ⅱ in HepG-2 cells was determined by enzyme-linked immunosorbent assay (ELISA).MTT assay was used to determine the effect of VitK₂ on the growth of HepG-2 cells.The effect of VitK₂ on the invasive ability of HepG-2 cells was determined by Transwell method. Results The positive rate of PIVKA-Ⅱ in hepatocellular carcinoma (74.0%) was higher than that in para-cancerous tissues (25.0%),P<0.05.The level of PIVKA-Ⅱ in hepatocellular carcinoma (3 786.23±143.24) mAU/g was higher than that in para-cancerous tissues (167.34±21.54) mAU/g (P<0.05).The level of PIVKA-Ⅱ in hepatocarcinoma cells in control group was (3.43±0.04) ng/(ml·10⁶ cells),the level of PIVKA-Ⅱ in VitK₂ group was (2.57±0.02) ng/(ml·10⁶ cells).The PIVKA-Ⅱ level in VitK₂ group was significantly lower than that in control group (P<0.05).On the 1st,2nd,3rd,4th,5th and 6th day of VitK₂ was co-cultured with HepG-2 cells,the inhibitory rates of VitK₂ on HepG-2 cells were 9.2%,16.5%,26.7%,34.8%,41.2% and 46.7%,respectively.After 24 h of VitK₂ was co-cultured with HepG-2 cells,VitK₂ on HepG-2 liver cancer cell invasion inhibition rate was 37.2%. Conclusion The expression of PIVKA-Ⅱ in hepatocellular carcinoma was high.VitK₂ can reduce the level of PIVKA-Ⅱ in hepatocarcinoma cells,inhibit the growth of hepatocarcinoma cells and reduce the invasiveness of HCC cells.
- Hepatocellular carcinoma /
- Vitamin K₂ /
- Vitamin K deficiency or antagonist-Ⅱ-induced protein