蜂毒素靶向PTEN/PI3K/Akt信号通路调控非小细胞肺癌细胞的增殖、凋亡

目的蜂毒素能否调控非小细胞肺癌细胞的增殖、凋亡,及其可能的作用机制。方法体外培养非小细胞肺癌细胞A549,在其中加入不同浓度蜂毒素进行干预(0、1、2、4 mg/L),MTT检测细胞增殖抑制率,Annexin V FITC/PI联合流式细胞仪检测细胞凋亡,Western Blot 检测细胞内PTEN、p-PI3K和p-Akt蛋白表达,RT-PCR检测细胞内p53和CyclinD1基因表达。结果蜂毒素能有效抑制A549细胞的增殖,促进细胞的凋亡,上调细胞PTEN的蛋白表达量,下调p-PI3K和p-Akt蛋白表达量,各浓度间差异具有统计学意义(P<0.05);蜂毒素能诱导p53 mRNA、抑制CyclinD1 mRNA的表达,各浓度间差异具有统计学意义(P<0.05)。结论蜂毒素能通过调控PTEN/PI3K/Akt信号通路抑制A549细胞的增殖,促进其凋亡。

Melittin Targeting PTEN/PI3K/Akt Signaling Pathway Regulates Proliferation and Apoptosis ofNon-small Cell Lung Cancer Cells

Objective To investigate whether melittin can regulate the proliferation and apoptosis of non-small celllung cancer cells and its possible mechanism.Methods Non-small cell lung cancer cells A549 were cultured in vitro,and different concentrations of melittin were added to intervene (0 mg/L,1 mg/L,2 mg/L,4 mg/L).MTT assay was used to detect cell proliferation inhibition rate,Annexin V FITC/PI.Apoptosis was detected by flow cytometry.The protein expressions of PTEN,p-PI3K and p-Akt were detected by Western Blot.The genes expressions of p53 and CyclinD1 were detected by RT-PCR.Results Melittin could effectively inhibit the proliferation of A549 cells,promotecell apoptosis,up-regulate the protein expression of PTEN,and down-regulate the expression of p-PI3K and p-Aktprotein.The difference between the concentrations was statistically significant (P<0.05).Melittin can promote p53 mRNA and inhibit the expression of CyclinD1 mRNA,and the difference between the concentrations is statistically significant (P<0.05).Conclusion Melittin can inhibit the proliferation and promote the apoptosis of A549 cells byregulating PTEN/PI3K/Akt signaling pathway.