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首页> 外文期刊>Life sciences >Substituted diaryl diselenides: Cytotoxic and apoptotic effect in human colon adenocarcinoma cells
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Substituted diaryl diselenides: Cytotoxic and apoptotic effect in human colon adenocarcinoma cells

机译：取代的二芳基二硒化物：对人结肠腺癌细胞的细胞毒性和凋亡作用

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Aims: To investigate the effects and study the underlying cell death mechanisms of diaryl diselenides, including: diphenyl diselenide (C 6H 5Se) 2; 4-chlorodiphenyl diselenide (4-ClC 6H 4Se) 2; 3-(trifluoromethyl)-diphenyl diselenide (3-CF 3C 6H 4Se) 2 and 4-methoxydiphenyl diselenide (4-MeOC 6H 4Se) 2, on the human colon adenocarcinoma cell line HT-29. Main methods: The viability of HT-29 cells after exposure to the diaryl diselenides and its substituted structures was based on the MTT assay. To verify if cell death was mediated throughout apoptosis mechanisms, flow cytometry and real-time PCR (qPCR) analyses were conducted. Key findings: The MTT assay and flow cytometry analyses showed that (3-CF 3C 6H 4Se) 2 and (4-MeOC 6H 4Se) 2 induced cytotoxicity through apoptosis mechanisms in HT-29 cells. qPCR revealed there was an up-regulation of pro-apoptotic (Bax, casapase-9, caspase-8, apoptosis-inducing factor (AIF) and Endonuclease G (EndoG)) and cell-cycle arrest genes (p53 and p21) and down-regulation of anti-apoptotic (Bcl-2 and survivin) and Myc genes. Significance: These results demonstrate that (3-CF 3C 6H 4Se) and (4-MeOC 6H 4Se) 2 have the potential to induce apoptosis in HT-29 cells through the activation of caspase-dependent and independent pathways and through cell-cycle arrest.
机译：目的：研究二芳基二硒化物的作用并研究其潜在的细胞死亡机制，包括：二苯基二硒化物（C 6H 5Se）2; 4-氯二苯基二硒化物（4-ClC 6H 4Se）2;在人结肠腺癌细胞系HT-29上的3-（三氟甲基）-二苯基二硒化物（3-CF 3C 6H 4Se）2和4-甲氧基二苯基二硒化物（4-MeOC 6H 4Se）2。主要方法：HT-29细胞暴露于二芳基二硒化物及其取代结构后的活力基于MTT分析。为了验证是否在整个凋亡机制中介导了细胞死亡，进行了流式细胞仪和实时PCR（qPCR）分析。主要发现：MTT分析和流式细胞仪分析表明（3-CF 3C 6H 4Se）2和（4-MeOC 6H 4Se）2通过HT-29细胞的凋亡机制诱导细胞毒性。 qPCR显示凋亡前体（Bax，casapase-9，caspase-8，凋亡诱导因子（AIF）和核酸内切酶G（EndoG））和细胞周期阻滞基因（p53和p21）上调并下调调节抗凋亡蛋白（Bcl-2和survivin）和Myc基因。意义：这些结果表明，（3-CF 3C 6H 4Se）和（4-MeOC 6H 4Se）2具有激活caspase依赖性和独立途径以及通过细胞周期停滞来诱导HT-29细胞凋亡的潜力。 。

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