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人β-防御素-1激活人结肠癌细胞中的自噬——长链非编码RNA TCONS_00014506的调控

Human β-defensin-1 activates autophagy in human colon cancer cells regulation of long non-coding RNA TCONS_00014506.

作者信息

Eid Nabil, Davamani Fabian

机构信息

Anatomy Department, Division of Human Biology, School of Medicine, International Medical University, Kuala Lumpur 57000, Malaysia.

Division of Applied Biomedical Sciences and Biotechnology, School of Health Sciences, International Medical University, Kuala Lumpur 57000, Malaysia.

出版信息

World J Gastrointest Oncol. 2024 Jul 15;16(7):2894-2901. doi: 10.4251/wjgo.v16.i7.2894.

Abstract

Macroautophagy (hereafter referred to as autophagy) is a prosurvival mechanism for the clearance of damaged cellular components, specifically related to exposure to various stressors such as starvation, excessive ethanol intake, and chemotherapy. This editorial reviews and comments on an article by Zhao , to be published in in 2024. Based on various molecular biology methodologies, they found that human β-defensin-1 reduced the proliferation of colon cancer cells, which was associated with the inhibition of the mammalian target of rapamycin, resulting in autophagy activation. The activation of autophagy is evidenced by increased levels of Beclin1 and LC3II/I proteins and mediated by the upregulation of long non-coding RNA TCONS_00014506. Our study discusses the impact of autophagy activation and mechanisms of autophagy, including autophagic flux, on cancer cells. Additionally, we emphasize the importance of describing the detailed methods for isolating long noncoding RNAs TCONS_00014506. Our review will benefit the scientific community and improve the overall clarity of the paper.

摘要

巨自噬(以下简称自噬)是一种清除受损细胞成分的促生存机制,特别与暴露于各种应激源(如饥饿、过量摄入乙醇和化疗)有关。这篇社论对赵等人将于2024年发表的一篇文章进行了综述和评论。基于各种分子生物学方法,他们发现人类β-防御素-1可降低结肠癌细胞的增殖,这与抑制雷帕霉素靶蛋白有关,从而导致自噬激活。自噬的激活通过Beclin1和LC3II/I蛋白水平的升高得以证明,并由长链非编码RNA TCONS_00014506的上调介导。我们的研究讨论了自噬激活及其机制(包括自噬通量)对癌细胞的影响。此外,我们强调了描述分离长链非编码RNA TCONS_00014506详细方法的重要性。我们的综述将使科学界受益,并提高论文的整体清晰度。

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