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自噬在癌症从传统递药系统向新型递药系统发展中的双重作用。

Dual role of autophagy for advancements from conventional to new delivery systems in cancer.

机构信息

Shobhaben Pratapbhai Patel School of Pharmacy and Technology Management, SVKM'S NMIMS, V. L. Mehta Road, Vile Parle (W), Mumbai, India.

Shobhaben Pratapbhai Patel School of Pharmacy and Technology Management, SVKM'S NMIMS, V. L. Mehta Road, Vile Parle (W), Mumbai, India.

出版信息

Biochim Biophys Acta Gen Subj. 2023 Oct;1867(10):130430. doi: 10.1016/j.bbagen.2023.130430. Epub 2023 Jul 26.


DOI:10.1016/j.bbagen.2023.130430
PMID:37506854
Abstract

Autophagy, a programmed cell-lysis mechanism, holds significant promise in the prevention and treatment of a wide range of conditions, including cancer, Alzheimer's, and Parkinson's disease. The successful utilization of autophagy modulation for therapeutic purposes hinges upon accurately determining the role of autophagy in disease progression, whether it acts as a cytotoxic or cytoprotective factor. This critical knowledge empowers scientists to effectively manipulate tumor sensitivity to anti-cancer therapies through autophagy modulation, while also circumventing drug resistance. However, conventional therapies face limitations such as low bioavailability, poor solubility, and a lack of controlled release mechanisms, hindering their clinical applicability. In this regard, innovative nanoplatforms including organic and inorganic systems have emerged as promising solutions to offer stimuli-responsive, theranostic-controlled drug delivery systems with active targeting and improved solubility. The review article explores a variety of organic nanoplatforms, such as lipid-based, polymer-based, and DNA-based systems, which incorporate autophagy-inhibiting drugs like hydroxychloroquine. By inhibiting the glycolytic pathway and depriving cells of essential nutrients, these platforms exhibit tumor-suppressive effects in advanced forms of cancer such as leukemia, colon cancer, and glioblastoma. Furthermore, metal-based, metal-oxide-based, silica-based, and quantum dot-based nanoplatforms selectively induce autophagy in tumors, leading to extensive cancer cell destruction. Additionally, this article discusses the current clinical status of autophagy-modulating drugs for cancer therapy with valuable insights of progress and potential of such approaches.

摘要

自噬是一种程序性细胞裂解机制,在预防和治疗多种疾病方面具有很大的应用前景,包括癌症、阿尔茨海默病和帕金森病等。要成功地将自噬调控应用于治疗目的,关键是要准确确定自噬在疾病进展中的作用,它是作为细胞毒性还是细胞保护因子发挥作用。这一关键知识使科学家能够通过自噬调控有效地操纵肿瘤对癌症治疗的敏感性,同时避免耐药性的产生。然而,传统疗法面临着一些局限性,如生物利用度低、溶解度差以及缺乏控制释放机制等,这限制了它们的临床应用。在这方面,包括有机和无机系统在内的创新纳米平台已经成为有前途的解决方案,可以提供刺激响应、治疗控制的药物输送系统,具有主动靶向和提高溶解度的特性。这篇综述文章探讨了多种有机纳米平台,如基于脂质、聚合物和 DNA 的系统,这些系统可以将自噬抑制药物如羟氯喹纳入其中。通过抑制糖酵解途径并剥夺细胞必需的营养物质,这些平台在白血病、结肠癌和神经胶质瘤等晚期癌症中表现出肿瘤抑制作用。此外,基于金属、金属氧化物、硅基和量子点的纳米平台可以选择性地诱导肿瘤中的自噬,导致广泛的癌细胞破坏。此外,本文还讨论了目前用于癌症治疗的自噬调节药物的临床现状,以及这些方法的进展和潜力的宝贵见解。

相似文献

[1]
Dual role of autophagy for advancements from conventional to new delivery systems in cancer.

Biochim Biophys Acta Gen Subj. 2023-10

[2]
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[3]
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[4]
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[5]
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[6]
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[7]
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[8]
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[9]
Nano delivery of natural substances as prospective autophagy modulators in glioblastoma.

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[10]
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引用本文的文献

[1]
The Effect of Arsenic Trioxide and Its Combination with Oxaliplatin and Docetaxel on the Induction of Autophagy and Expression of LC3 and Beclin-1 Genes in AGS and MKN-45 Gastric Cancer Cell Lines.

Adv Pharm Bull. 2024-12-5

[2]
Glycopolymer nanomicelles: pH-responsive drug delivery, endocytosis pathway, autophagy behavior, and the effect of autophagy inhibitors.

J Mater Sci Mater Med. 2025-6-6

[3]
RNA-binding proteins and autophagy in lung cancer: mechanistic insights and therapeutic perspectives.

Discov Oncol. 2025-4-24

[4]
Autophagy: a double-edged sword in ischemia-reperfusion injury.

Cell Mol Biol Lett. 2025-4-7

[5]
Alpha-Lipoic Acid Reduces Cell Growth, Inhibits Autophagy, and Counteracts Prostate Cancer Cell Migration and Invasion: Evidence from In Vitro Studies.

Int J Mol Sci. 2023-12-4

[6]
Unraveling the Janus-Faced Role of Autophagy in Hepatocellular Carcinoma: Implications for Therapeutic Interventions.

Int J Mol Sci. 2023-11-13

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