TAT修饰短肽LVKEI抑制黑色素瘤B16细胞增殖及促凋亡作用

TAT-modified short peptide LVKEI inhibits proliferation of melanoma B16 cells and its apoptotic effect

  • 摘要: 目的 探讨TAT修饰短肽LVKEI(TAT-LVKEI)对黑色素瘤B16细胞增殖及凋亡的影响。 方法 采用CCK-8检测细胞增殖活力,采用流式细胞仪检测细胞周期、细胞凋亡率,采用Western-blotting检测凋亡相关蛋白表达。 结果 TAT-LVKEI能抑制黑色素瘤细胞系B16细胞的增殖活力并将细胞周期阻滞于G0/G1期; TAT-LVKEI能诱导黑色素瘤细胞系B16细胞凋亡; TAT-LVKEI处理可增加Cleaved Caspase-3、Bax的表达水平,降低Bcl2、Ki-67的表达水平。 结论 TAT-LVKEI能抑制B16黑色素瘤细胞增殖并促使其凋亡。

     

    Abstract: Objective To explore the effect of TAT-modified short peptide LVKEI(TAT-LVKEI)on the proliferation and apoptosis of melanoma B16 cells. Methods The CCK-8 kit was used to detect cell proliferation viability, flow cytometry was used to detect cell cycle and cell apoptosis, and Western-blotting was used to detect apoptosis-related protein expression. Results TAT-LVKEI was able to inhibit the proliferation viability of melanoma cell line B16 cells and arrest cell cycle at G0/G1 phase. TAT-LVKEI was able to induce apoptosis of melanoma cell line B16 cells. TAT-LVKEI management was able to increase the expression levels of Cleaved Caspase-3 and Bax, and decrease expression levels of Bcl2 and Ki-67. Conclusion TAT-LVKEI can inhibit proliferation and promote apoptosis of melanoma B16 cells.

     

/

返回文章
返回