首页|激活蛋白激酶B/鼠双微体基因2/p53信号通路抑制非小细胞肺癌H1975细胞增殖和侵袭

激活蛋白激酶B/鼠双微体基因2/p53信号通路抑制非小细胞肺癌H1975细胞增殖和侵袭

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目的 观察调控蛋白激酶B(Akt)/鼠双微体基因2(MDM2)/p53信号通路对非小细胞肺癌(NSCLC)恶性生物学行为的影响.方法 取对数期H1975细胞株(美国类型培养物保藏中心),分别用 Akt/MDM2/p53 信号通路激活剂 SC79(4μg/ml)、抑制剂 perifosine(5.0 μmol/L)处理,设为SC79组、perifosine组,取不做任何处理的H1975细胞株设为空白组.干预24 h检测细胞增殖能力、凋亡率及侵袭能力.多组间比较用单因素方差分析,两组间比较用LSD-t检验.结果 SC79组 24、48、72h 吸光度值(0.38±0.05、0.63±0.07、0.89±0.12)高于空白组(0.25±0.04、0.46±0.07、0.62±0.11,t=4.540、3.840、3.709,P<0.01);perifosine 组 24、48、72 h 吸光度值(0.16±0.04、0.29±0.06、0.40±0.09)低于空白组(0.25±0.04、0.46±0.07、0.62±0.11,t=3.558、4.123、3.461,P<0.01).SC79组凋亡率[(2.01±0.57)%]低于空白组[(3.21±0.74)%,t=2.813,P<0.05];perifosine 组凋亡率[(12.38±3.01)%]高于空白组[(3.21±0.74)%,t=7.569,P<0.01].SC79组每个视野透膜细胞数量(95.20±15.62)高于空白组(54.80±9.13,t=4.993,P<0.05);perifosine组每个视野透膜细胞数量(30.40±8.41)低于空白组(54.80±9.13,t=4.395,P<0.01).结论 激活Akt/MDM2/p53信号通路可促进NSCLC细胞增殖、侵袭,抑制其凋亡.
Activation of protein kinase B/murine double minute 2/p53 signaling pathway inhibits proliferation and invasion of non-small cell lung cancer H1975 cells
Objective To observe the effect of regulating the protein kinase B(Akt)/mouse doub-le minute 2(MDM2)/p53 signaling pathway on the malignant biological behavior of non-small cell lung cancer(NSCLC).Methods Logarithmic phase H1975 cell lines(purchased from the U.S.Type Culture Preservation Center)were treated with the Akt/MDM2/p53 signaling pathway activator SC79(4 μg/ml)and inhibitor perifosine(5.0 μmol/L),designated as the SC79 group and perifosine group,respectively.Cells from the untreated H1975 line were used as the control group.The H1975 cell line without any treat-ment was set as blank group.Cell proliferation,apoptosis rate and invasion ability were detected after 24 h intervention.One-way ANOVA was used for comparison among multiple groups and LSD-t test was used for comparison between two groups.Results The absorbance values at 24,48 and 72 h in SC79 group(0.38±0.05,0.63±0.07,0.89±0.12)were higher than those in blank group(0.25±0.04,0.46±0.07,0.62±0.11,t=4.540,3.840,3.709,P<0.01).The absorbance values in perifosine group at 24,48 and 72 h(0.16±0.04,0.29±0.06,0.40±0.09)were lower than those in blank group(0.25±0.04,0.46±0.07,0.62±0.11,t=3.558,4.123,3.461,P<0.01).The apoptosis rate[(2.01±0.57)%]in SC79 group was lower than that in blank group[(3.21±0.74)%,t=2.813,P<0.05].The apoptosis rate in perifosine group[(12.38±3.01)%]was higher than that in blank group[(3.21±0.74)%,t=7.569,P<0.01].The number of transmembrane cells per field in SC79 group(95.20±15.62)was greater than that in blank group(54.80±9.13,t=4.993,P<0.05).The number of cells in perifosine group(30.40±8.41)was less than that in blank group(54.80±9.13,t=4.395,P<0.01).Conclusion Activation of Akt/MDM2/p53 signaling pathway can promote proliferation and invasion,and inhibit apoptosis of NSCLC cells.

Protein kinase BDouble minute 2Non-small cell lung cancerProliferationInvasion

潘宇、傅静云、陈涛

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三峡大学基础医学院,宜昌 443000

蛋白激酶B 双微体基因2 非小细胞肺癌 增殖 侵袭

国家自然科学基金

81873148

2024

中华实验外科杂志
中华医学会

中华实验外科杂志

CSTPCD
影响因子:0.759
ISSN:1001-9030
年,卷(期):2024.41(6)
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