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新疆医科大学附属肿瘤医院麻醉科
Published:2025
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[1]袁婷婷,阿迪莱·库热西,闫睿.丙泊酚通过miR-21/PTEN通路抑制结肠癌HCT116细胞增殖[J].新疆大学学报(自然科学版中英文),2025,42(05):632-640.
[1]袁婷婷,阿迪莱·库热西,闫睿.丙泊酚通过miR-21/PTEN通路抑制结肠癌HCT116细胞增殖[J].新疆大学学报(自然科学版中英文),2025,42(05):632-640. DOI: 10.13568/j.cnki.651094.651316.2025.04.20.0002.
DOI:10.13568/j.cnki.651094.651316.2025.04.20.0002.
结肠癌作为全球高发的恶性肿瘤,其发病率和死亡率均位居癌症前列.麻醉药物丙泊酚在多种癌症中表现出抗肿瘤活性,其作用机制可能与调节miR-21的表达相关.本文重点关注丙泊酚通过调控miR-21-5p/PTEN信号通路对结肠癌细胞增殖和凋亡的影响机制,为结肠癌治疗提供新的潜在靶点.将HCT116细胞分为对照组、丙泊酚组、miR-21-5p NC组、miR-21-5p mimic组、丙泊酚+miR-21-5p NC组、丙泊酚+miR-21-5p mimic组,将miR-21-5p mimic或miR-21-5p NC转染至HCT116细胞后,使用CCK-8法检测细胞增殖,流式细胞仪检测细胞周期,qRT-PCR检测细胞中miR-21-5p和PTEN的基因表达,Western Blot(WB)检测PTEN、p-AKT等关键蛋白的表达,双荧光素酶基因报告实验检测miR-21-5p与PTEN的靶向关系.实验结果显示:与对照组相比,丙泊酚处理显著抑制HCT116细胞增殖.在分子机制方面,丙泊酚组miR-21-5p mRNA表达水平较对照组显著下调,同时伴随PTEN mRNA表达水平增加(P<0.05).WB分析表明:miR-21-5p过表达可抑制PTEN蛋白表达并激活p-AKT信号,而丙泊酚处理能够逆转这一效应.双荧光素酶报告实验进一步证实,PTEN是miR-21-5p的靶基因.故丙泊酚可能通过抑制miR-21-5p,解除其对PTEN的靶向调控作用,从而影响细胞增殖.
As a highly prevalent malignant tumor worldwide
colon cancer ranks among the top cancers in terms of morbidity and mortality.The anesthetic drug propofol exhibits antitumor activity in a variety of cancers
and its mechanism of action may be related to the regulation of miR-21 expression.The paper focuses on the effects of propofol on colon cancer cell proliferation and apoptosis by modulating the miR-21-5p/PTEN signaling pathway
aiming to reveal this molecular mechanism to provide new potential targets for colon cancer therapy.HCT116 cells are divided into control group
propofol group
miR-21-5p NC group
miR-21-5p mimic group
propofol+miR-21-5p NC group
propofol+miR-21-5p mimic group
and miR-21-5p mimic or miR-21-5p NC are transfected into HCT116cells
and CCK-8 method is used to detect cell proliferation
flow cytometry is used to detect cell cycle.qRT-PCR is used to detect gene expression of miR-21-5p and PTEN in cells.Western Blot(WB) is used to detect the expression of key proteins such as PTEN and p-AKT.A dual luciferase gene reporter assay is used to detect the targeting relationship between miR-21-5p and PTEN.The experimental results show that propofol treatment significantly inhibites the proliferation of HCT116 cells compared with the control group.In terms of molecular mechanisms
miR-21-5p mRNA expression level is significantly down-regulated in the propofol group compared with the control group
accompanied by an increase in PTEN mRNA expression level(P<0.05).WB analysis shows that miR-21-5p overexpression inhibites PTEN protein expression and activates p-AKT signaling
and propofol treatment is able to reverse this effect.Dual luciferase reporter assay further confirms that PTEN is a target gene of miR-21-5p.It is suggested that propofol may affect cell proliferation by inhibiting miR-21-5p and deregulating its targeted regulation of PTEN.
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