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口腔癌中的自噬:前景与挑战(综述)。

Autophagy in oral cancer: Promises and challenges (Review).

机构信息

Department of Stomatology, First Hospital of Shanxi Medical University, Taiyuan, Shanxi 030000, P.R. China.

Shanxi Key Laboratory of Oral Diseases Prevention and New Materials, Shanxi Medical University School and Hospital of Stomatology, Taiyuan, Shanxi 030000, P.R. China.

出版信息

Int J Mol Med. 2024 Dec;54(6). doi: 10.3892/ijmm.2024.5440. Epub 2024 Oct 18.


DOI:10.3892/ijmm.2024.5440
PMID:39422076
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11518578/
Abstract

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.

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,以实现适当的细胞内稳态。自噬具有独特的特征,并在许多生理和病理条件下具有公认的功能,如癌症。自噬可以阻止早期癌症的发展。在肿瘤细胞成功转化并进展到晚期后,自噬介导的动态降解和再循环系统将支持癌细胞生长和适应各种细胞应激反应,同时保持能量内稳态。本研究综述了自噬在各种口腔癌发展背景和阶段中的双重作用、自噬的现有正反两方面观点,以及自噬在口腔癌发生、耐药性、侵袭、转移和自我增殖等方面的作用机制和功能。特别关注自噬在口腔癌过程中的机制和功能,以及将某些常规药物或天然化合物作为新型药物应用于调节口腔癌自噬的最新发现。总的来说,需要进一步研究以确定促进和抑制自噬的有效性和可靠性,同时最大限度地增加增加癌症抑制的难度挑战,以改善临床结果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17b6/11518578/53457169f706/ijmm-54-06-05440-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17b6/11518578/f6f197e21c4a/ijmm-54-06-05440-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17b6/11518578/49f1efd7d65c/ijmm-54-06-05440-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17b6/11518578/97ad8ce87e85/ijmm-54-06-05440-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17b6/11518578/56ca150b6fbd/ijmm-54-06-05440-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17b6/11518578/53457169f706/ijmm-54-06-05440-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17b6/11518578/f6f197e21c4a/ijmm-54-06-05440-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17b6/11518578/49f1efd7d65c/ijmm-54-06-05440-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17b6/11518578/97ad8ce87e85/ijmm-54-06-05440-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17b6/11518578/56ca150b6fbd/ijmm-54-06-05440-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17b6/11518578/53457169f706/ijmm-54-06-05440-g04.jpg

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引用本文的文献

[1]
ER‑α36 knockdown is associated with lysosomal dysfunction and proliferation inhibition in liver cancer cells.

Mol Med Rep. 2025-10

[2]
Therapeutic Targeting of Apoptosis, Autophagic Cell Death, Necroptosis, Pyroptosis, and Ferroptosis Pathways in Oral Squamous Cell Carcinoma: Molecular Mechanisms and Potential Strategies.

Biomedicines. 2025-7-16

[3]
A bibliometric analysis of programmed cell death in oral cancer literature: research patterns and emerging trends (2000-2024).

Discov Oncol. 2025-4-22

[4]
Beyond Genetics: Exploring Lifestyle, Microbiome, and Social Determinants in Oral Cancer Development.

Cancers (Basel). 2025-3-25

[5]
Elevated neuregulin‑1 expression modulates tumor malignancy and autophagy in esophageal squamous cell carcinoma.

Int J Mol Med. 2025-4

[6]
Targeting autophagy to enhance chemotherapy and immunotherapy in oral cancer.

Front Immunol. 2025-1-7

本文引用的文献

[1]
25 year trends in cancer incidence and mortality among adults aged 35-69 years in the UK, 1993-2018: retrospective secondary analysis.

BMJ. 2024-3-13

[2]
Piperine Induces Apoptosis and Autophagy in HSC-3 Human Oral Cancer Cells by Regulating PI3K Signaling Pathway.

Int J Mol Sci. 2023-9-11

[3]
Piperlongumine Induces Apoptosis and Cytoprotective Autophagy via the MAPK Signaling Pathway in Human Oral Cancer Cells.

Biomedicines. 2023-9-1

[4]
Spermidine Suppresses Oral Carcinogenesis through Autophagy Induction, DNA Damage Repair, and Oxidative Stress Reduction.

Am J Pathol. 2023-12

[5]
Chaperone-mediated autophagy: Molecular mechanisms, biological functions, and diseases.

MedComm (2020). 2023-8-30

[6]
Xanol Promotes Apoptosis and Autophagy and Inhibits Necroptosis and Metastasis via the Inhibition of AKT Signaling in Human Oral Squamous Cell Carcinoma.

Cells. 2023-7-3

[7]
Co-targeting autophagy and NRF2 signaling triggers mitochondrial superoxide to sensitize oral cancer stem cells for cisplatin-induced apoptosis.

Free Radic Biol Med. 2023-10

[8]
Caffeic Acid Phenethyl Ester and Caffeamide Derivatives Suppress Oral Squamous Cell Carcinoma Cells.

Int J Mol Sci. 2023-6-6

[9]
Synergistic Effects of New Curcumin Analog (PAC) and Cisplatin on Oral Cancer Therapy.

Curr Issues Mol Biol. 2023-6-8

[10]
Rhein Induces Oral Cancer Cell Apoptosis and ROS via Suppresse AKT/mTOR Signaling Pathway In Vitro and In Vivo.

Int J Mol Sci. 2023-5-9

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