期刊文献+

维生素K2联合5-氟尿嘧啶对肝癌细胞增殖、迁移与侵袭能力的影响

Effects of Vitamin K2 Plus 5-Fluorouracil on Proliferation, Migration, and Invasiveness of Hepatocellular Carcinoma Cells
原文传递
导出
摘要 目的探讨维生素K2(VK2)联合5-氟尿嘧啶(5-FU)对肝癌细胞体外增殖、迁移和侵袭的影响。方法体外培养人肝癌PLC/RAF/5细胞,分别用VK2(100μmol/L)、5-FU(10μg/m L)及VK2与5-FU联合用药处理细胞24 h,另设置不加药的细胞作为对照组,分别采用CCK-8法、划痕试验、Matrigel侵袭小室法检测细胞增殖、迁移及侵袭情况。结果 VK2或5-FU单独作用细胞后,PLC/RAF/5细胞增殖、迁移和侵袭能力较对照组均明显降低(P<0.05);而与任一单独用药比较,VK2与5-FU联合用药对细胞增殖、迁移和侵袭能力的抑制作用均进一步明显增强(P<0.05)。结论 VK2与5-FU联合应用可能成为抑制肝癌细胞生长、迁移和侵袭的有效方法。 Objective To investigate effects of vitamin K2 in combination with 5-fluorouracil (5-FU) on proliferation, migration, and invasiveness of hepatocellular carcinoma cells in vitro. Methods Human hepatocellular carcinoma PLC/RAF/5 calls were cultured in vitro and exposed to vitamin K2 (10 μmol/L) and 5-FU (10 μg/mL) alone or in combination for 24 h. The cell proliferation, migration, and invasiveness were measured by CCK-8 assay, wound-cratch assay, and Matrigel invasion chamber assay, respectively. Results The abilities of proliferation, migration, and invasion of PLC/RAF/5 cells were significantly decreased after either alone vitamin K2 or 5-FU treatment (all P〈0.05) as compared with the control ceils, and above effects were further enhanced by the vitamin K2 in combination with 5-FU treatment as compared with either alone drug treatment (all P〈0.05). Conclusion Combination use of vitamin K2 and 5-FU might be an effective method for inhibiting growth, migration, and invasiveness of hepatocellular carcinoma cells.
出处 《中国普外基础与临床杂志》 CAS 2016年第11期1321-1324,共4页 Chinese Journal of Bases and Clinics In General Surgery
关键词 肝细胞癌 维生素K2 5-氟尿嘧啶 化疗方案 Hepatocellular carcinoma Vitamin K2 5-fluorouracil Chemotherapy protocol
  • 相关文献

参考文献2

二级参考文献24

  • 1Nishikawa T, Tsuno NH, Okaji Y, et al. Inhibition of autophagy potentiates sulforaphane-induced apoptosis in human colon cancer cells[J]. Ann Surg Oncol, 2010, 17(2): 592-602.
  • 2Li J, Hou N, Failed A, et al. Inhibition of autophagy augments 5-fluorouracil chemotherapy in human colon cancer in vitro and in vivo model [ J ]. Eur J Cancer, 2010, 46(10) : 1900-1909.
  • 3Kanematsu S, Uehara N, Miki H, et al. Autophagy inhibition enhances sulforaphane-induced apoptosis in human breast cancer cells [J]. Anticancer Res, 2010, 30(9): 3381-3390.
  • 4Liu D, Yang Y, Liu Q, et al. Inhibition of autophagy by 3-MA potentiates cisplatin-induced apoptosis in esophageal squamous cell carcinoma cells [J]. Med Oncol, 2011,28(1): 105-111.
  • 5Shimizu S, Takehara T, Hikita H, et al. Inhibition of autophagy potentiates the antitumor effect of the multikinase inhibitor sorafenib in hepatocellular carcinoma [J]. Int J Cancer, 2012, 131(3): 548-557.
  • 6Hsieh MJ, Yang SF, Hsieh YS, et al. Autophagy inhibition enhances apoptosis induced by dioscin in huh'/ cells [J]. Evid Based Complement Altemat Med, 2012, 2012: 134512.
  • 7Clark HP, Carson WF, Kavanagh PV, et al. Staging and current treatment ofhepatocellular carcinoma [J]. Radiographics, 2005, 25 Suppl 1 : $3-$23.
  • 8Chen S, Rehman SK, Zhang W, et al. Autophagy is a therapeutic target in anticancer drug resistance [J]. Biochim Biophys Acta, 2010, 1806(2): 220-229.
  • 9Hu YL, Jahangiri A, Delay M, et al. Tumor cell autophagy as an adaptive response mediating resistance to treatments such as antiangiogenic therapy [J]. Cancer Res, 2012, 72(17): 4294- 4299.
  • 10Lin JF, Tsai TF, Liao PC, et al. Benzyl isothiocyanate induces protective autophagy in human prostate cancer cells via inhibition ofmTOR signaling [J]. Carcinogenesis, 2013, 34(2): 406-414.

共引文献6

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部