Humanβ-defensin-1 activates autophagy in human colon cancer cells via regulation of long non-coding RNA TCONS_00014506  被引量:1

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作  者:Nabil Eid Fabian Davamani 

机构地区:[1]Anatomy Department,Division of Human Biology,School of Medicine,International Medical University,Kuala Lumpur 57000,Malaysia [2]Division of Applied Biomedical Sciences and Biotechnology,School of Health Sciences,International Medical University,Kuala Lumpur 57000,Malaysia

出  处:《World Journal of Gastrointestinal Oncology》2024年第7期2894-2901,共8页世界胃肠肿瘤学杂志(英文)

摘  要: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 humanβ-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.

关 键 词:Colon cancer Humanβ-defensin-1 Long noncoding RNA Mammalian target of rapamycin AUTOPHAGY LC3-II BECLIN-1 Autophagy flux 

分 类 号:R735.34[医药卫生—肿瘤]

 

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