Melittin 作为结直肠 HCT116 细胞株自噬和折叠蛋白反应途径的激活剂

Q2 Biochemistry, Genetics and Molecular Biology
Iranian Biomedical Journal Pub Date : 2024-01-01 Epub Date: 2023-11-21 DOI:10.61186/ibj.3993
Mozhdeh Zamani, Farzaneh Bozorg-Ghalati, Pooneh Mokarram
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引用次数: 0

摘要

背景:甜菊素的潜在抗癌作用促使科学家们寻找其确切的分子作用机制。UPR和自噬是参与结直肠癌肿瘤发生和耐药性的两条关键通路,有关美乐汀对这两条通路影响的数据很少。本研究旨在探讨美乐汀对 CRC HCT116 细胞中这些通路的影响:在选择了最佳浓度和处理时间后,采用qRT-PCR检测自噬通路标志物(LC3-βII和P62)和UPR标志物(CHOP和XBP-1s)的基因表达。此外,还通过 Western 印迹法测定了自噬启动标记物(Beclin1)的蛋白水平:结果:MTT检测显示美利曲丁对HCT116细胞有细胞毒性作用。LC3-βII表达水平的升高和P62 mRNA表达水平的降低以及Beclin1蛋白水平的升高表明美乐汀对自噬有促进作用。美利汀还能明显提高CHOP和XBP-1s在mRNA水平的表达,表明美利汀对UPR的激活具有积极作用:本研究表明,UPR和自噬可能被认为是肿瘤发生过程中的两条关键信号通路,BV美利汀可以靶向作用于HCT116细胞。建议进一步进行体内评估,以验证所获得的结果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Melittin as an Activator of the Autophagy and Unfolded Protein Response Pathways in Colorectal HCT116 Cell Line.

Background: The potential anticancer effect of melittin has motivated scientists to find its exact molecular mechanism of action. There are few data on the effect of melittin on the UPR and autophagy as two critical pathways involved in tumorigenesis of colorectal and drug resistance. This study aimed to investigate the effect of melittin on these pathways in the colorectal cancer (CRC) HCT116 cells.

Methods: MTT method was carried out to assess the cytotoxicity of melittin on the HCT116 cell line for 24, 48, and 72 h. After selecting the optimal concentrations and treatment times, the gene expression of autophagy flux markers (LC3-βII and P62) and UPR markers (CHOP and XBP-1s) were determined using qRT-PCR. The protein level of autophagy initiation marker (Beclin1) was also determined by Western blotting.

Results: MTT assay showed a cytotoxic effect of melittin on the HCT116 cells. The increase in LC3-βII and decrease in P62 mRNA expression levels, along with the elevation in the Beclin1 protein level, indicated the stimulatory role of melittin on the autophagy. Melittin also significantly enhanced the CHOP and XBP-1s expressions at mRNA level, suggesting the positive role of the melittin on the UPR activation.

Conclusion: This study shows that UPR and autophagy can potentially be considered as two key signaling pathways in tumorigenesis, which can be targeted by the BV melittin in the HCT116 cells. Further in vivo evaluations are recommended to verify the obtained results.

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来源期刊
Iranian Biomedical Journal
Iranian Biomedical Journal Biochemistry, Genetics and Molecular Biology-Biochemistry, Genetics and Molecular Biology (all)
CiteScore
3.20
自引率
0.00%
发文量
42
审稿时长
8 weeks
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