自噬在口腔癌中的作用:前景与挑战(综述)。

IF 8.3 2区 材料科学 Q1 MATERIALS SCIENCE, MULTIDISCIPLINARY
ACS Applied Materials & Interfaces Pub Date : 2024-12-01 Epub Date: 2024-10-18 DOI:10.3892/ijmm.2024.5440
Zhou Li, Yao Zhang, Jianhua Lei, Yunxia Wu
{"title":"自噬在口腔癌中的作用:前景与挑战(综述)。","authors":"Zhou Li, Yao Zhang, Jianhua Lei, Yunxia Wu","doi":"10.3892/ijmm.2024.5440","DOIUrl":null,"url":null,"abstract":"<p><p>Autophagy captures damaged or dysfunctional proteins and organelles through the lysosomal pathway to achieve proper cellular homeostasis. Autophagy possesses distinct characteristics and is given recognized functions in numerous physiological and pathological conditions, such as cancer. Early stage cancer development can be stopped by autophagy. After tumor cells have successfully undergone transformation and progressed to a late stage, the autophagy-mediated system of dynamic degradation and recycling will support cancer cell growth and adaptation to various cellular stress responses while preserving energy homeostasis. In the present study, the dual function that autophagy plays in various oral cancer development contexts and stages, the existing arguments for and against autophagy, and the ways in which autophagy contributes to oral cancer modifications, such as carcinogenesis, drug resistance, invasion, metastasis and self-proliferation, are reviewed. Special attention is paid to the mechanisms and functions of autophagy in oral cancer processes, and the most recent findings on the application of certain conventional drugs or natural compounds as novel agents that modulate autophagy in oral cancer are discussed. Overall, further research is needed to determine the validity and reliability of autophagy promotion and inhibition while maximizing the difficult challenge of increasing cancer suppression to improve clinical outcomes.</p>","PeriodicalId":5,"journal":{"name":"ACS Applied Materials & Interfaces","volume":null,"pages":null},"PeriodicalIF":8.3000,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11518578/pdf/","citationCount":"0","resultStr":"{\"title\":\"Autophagy in oral cancer: Promises and challenges (Review).\",\"authors\":\"Zhou Li, Yao Zhang, Jianhua Lei, Yunxia Wu\",\"doi\":\"10.3892/ijmm.2024.5440\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Autophagy captures damaged or dysfunctional proteins and organelles through the lysosomal pathway to achieve proper cellular homeostasis. Autophagy possesses distinct characteristics and is given recognized functions in numerous physiological and pathological conditions, such as cancer. Early stage cancer development can be stopped by autophagy. After tumor cells have successfully undergone transformation and progressed to a late stage, the autophagy-mediated system of dynamic degradation and recycling will support cancer cell growth and adaptation to various cellular stress responses while preserving energy homeostasis. In the present study, the dual function that autophagy plays in various oral cancer development contexts and stages, the existing arguments for and against autophagy, and the ways in which autophagy contributes to oral cancer modifications, such as carcinogenesis, drug resistance, invasion, metastasis and self-proliferation, are reviewed. Special attention is paid to the mechanisms and functions of autophagy in oral cancer processes, and the most recent findings on the application of certain conventional drugs or natural compounds as novel agents that modulate autophagy in oral cancer are discussed. Overall, further research is needed to determine the validity and reliability of autophagy promotion and inhibition while maximizing the difficult challenge of increasing cancer suppression to improve clinical outcomes.</p>\",\"PeriodicalId\":5,\"journal\":{\"name\":\"ACS Applied Materials & Interfaces\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":8.3000,\"publicationDate\":\"2024-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11518578/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"ACS Applied Materials & Interfaces\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.3892/ijmm.2024.5440\",\"RegionNum\":2,\"RegionCategory\":\"材料科学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/10/18 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q1\",\"JCRName\":\"MATERIALS SCIENCE, MULTIDISCIPLINARY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Materials & Interfaces","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3892/ijmm.2024.5440","RegionNum":2,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/10/18 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"MATERIALS SCIENCE, MULTIDISCIPLINARY","Score":null,"Total":0}
引用次数: 0

摘要

自噬通过溶酶体途径捕获受损或功能失调的蛋白质和细胞器,以实现适当的细胞平衡。自噬具有鲜明的特点,在癌症等多种生理和病理情况下被赋予公认的功能。自噬可以阻止早期癌症的发展。在肿瘤细胞成功转化并发展到晚期阶段后,自噬介导的动态降解和循环系统将支持癌细胞生长和适应各种细胞应激反应,同时维持能量平衡。本研究综述了自噬在不同口腔癌发展背景和阶段中发挥的双重功能,现有的支持和反对自噬的论点,以及自噬如何促进口腔癌的癌变、耐药性、侵袭、转移和自我增殖等改变。特别关注了自噬在口腔癌过程中的机制和功能,并讨论了将某些常规药物或天然化合物作为新型药物应用于口腔癌自噬调节的最新发现。总之,需要进一步研究确定自噬促进和抑制的有效性和可靠性,同时最大限度地应对增加癌症抑制以改善临床疗效这一艰巨挑战。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Autophagy in oral cancer: Promises and challenges (Review).

Autophagy captures damaged or dysfunctional proteins and organelles through the lysosomal pathway to achieve proper cellular homeostasis. Autophagy possesses distinct characteristics and is given recognized functions in numerous physiological and pathological conditions, such as cancer. Early stage cancer development can be stopped by autophagy. After tumor cells have successfully undergone transformation and progressed to a late stage, the autophagy-mediated system of dynamic degradation and recycling will support cancer cell growth and adaptation to various cellular stress responses while preserving energy homeostasis. In the present study, the dual function that autophagy plays in various oral cancer development contexts and stages, the existing arguments for and against autophagy, and the ways in which autophagy contributes to oral cancer modifications, such as carcinogenesis, drug resistance, invasion, metastasis and self-proliferation, are reviewed. Special attention is paid to the mechanisms and functions of autophagy in oral cancer processes, and the most recent findings on the application of certain conventional drugs or natural compounds as novel agents that modulate autophagy in oral cancer are discussed. Overall, further research is needed to determine the validity and reliability of autophagy promotion and inhibition while maximizing the difficult challenge of increasing cancer suppression to improve clinical outcomes.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
ACS Applied Materials & Interfaces
ACS Applied Materials & Interfaces 工程技术-材料科学:综合
CiteScore
16.00
自引率
6.30%
发文量
4978
审稿时长
1.8 months
期刊介绍: ACS Applied Materials & Interfaces is a leading interdisciplinary journal that brings together chemists, engineers, physicists, and biologists to explore the development and utilization of newly-discovered materials and interfacial processes for specific applications. Our journal has experienced remarkable growth since its establishment in 2009, both in terms of the number of articles published and the impact of the research showcased. We are proud to foster a truly global community, with the majority of published articles originating from outside the United States, reflecting the rapid growth of applied research worldwide.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信