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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 et al, to be published in World J Gastrointestinal Oncology 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，特别是与各种压力因素如饥饿有关，过量的乙醇摄入，和化疗。这篇社论回顾和评论了赵等人的一篇文章，将于2024年在WorldJ胃肠肿瘤学上发表。基于各种分子生物学方法，他们发现人类β-防御素-1减少结肠癌细胞的增殖，这与哺乳动物雷帕霉素靶蛋白的抑制有关，导致自噬激活。自噬的激活由Beclin1和LC3II/I蛋白的水平增加证明，并且由长非编码RNATCONS_00014506的上调介导。我们的研究讨论了自噬激活的影响和自噬的机制，包括自噬通量，癌细胞。此外,我们强调描述分离长链非编码RNATCONS_00014506的详细方法的重要性。我们的审查将使科学界受益，并提高论文的整体清晰度。
