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评估大麻色烯、大麻二酚及来自[具体来源未给出]的相关化合物对恶性胶质瘤的抗肿瘤潜力:从计算机模拟到体外实验的方法。

Evaluating the Antitumor Potential of Cannabichromene, Cannabigerol, and Related Compounds from and Against Malignant Glioma: An In Silico to In Vitro Approach.

作者信息

Turizo Smith Andrés David, Montoya Moreno Nicolás, Rodríguez-García Josefa Antonia, Marín-Loaiza Juan Camilo, Arboleda Bustos Gonzalo

机构信息

Departamento de Patología, Facultad de Medicina, Universidad Nacional de Colombia, Bogotá 111221, Colombia.

Departamento de Química, Facultad de Ciencias, Universidad Nacional de Colombia, Bogotá 111221, Colombia.

出版信息

Int J Mol Sci. 2025 Jun 13;26(12):5688. doi: 10.3390/ijms26125688.

DOI:10.3390/ijms26125688
PMID:40565152
Abstract

Malignant gliomas, including glioblastoma multiforme (GBM), are highly aggressive brain tumors with a poor prognosis and limited treatment options. This study investigates the antitumor potential of bioactive compounds derived from and using molecular docking, cell viability assays, and transcriptomic and expression analyses from public databases in humans and cell lines. Cannabichromene (CBC), cannabigerol (CBG), cannabidiol (CBD), and Piper nigrum derivates exhibited strong binding affinities relative to glioblastoma-associated targets GPR55 and PINK1. In vitro analyses demonstrated their cytotoxic effects on glioblastoma cell lines (U87MG, T98G, and CCF-STTG1), as well as on neuroblastoma (SH-SY5Y) and oligodendroglial (MO3.13) cell lines, revealing interactions among these compounds. The differential expression of GPR55 and PINK1 in tumor versus normal tissues further supports their potential as biomarkers and therapeutic targets. These findings provide a basis for the development of novel therapies and suggest unexplored molecular pathways for the treatment of malignant glioma.

摘要

恶性胶质瘤,包括多形性胶质母细胞瘤(GBM),是具有高度侵袭性的脑肿瘤,预后较差且治疗选择有限。本研究利用分子对接、细胞活力测定以及来自人类和细胞系公共数据库的转录组和表达分析,研究了源自[具体物质1]和[具体物质2]的生物活性化合物的抗肿瘤潜力。大麻色烯(CBC)、大麻二醇(CBG)、大麻二酚(CBD)和黑胡椒衍生物相对于胶质母细胞瘤相关靶点GPR55和PINK1表现出很强的结合亲和力。体外分析证明了它们对胶质母细胞瘤细胞系(U87MG、T98G和CCF-STTG1)以及神经母细胞瘤(SH-SY5Y)和少突胶质细胞(MO3.13)细胞系的细胞毒性作用,揭示了这些化合物之间的相互作用。GPR55和PINK1在肿瘤组织与正常组织中的差异表达进一步支持了它们作为生物标志物和治疗靶点的潜力。这些发现为开发新疗法提供了依据,并为恶性胶质瘤的治疗提示了未被探索的分子途径。

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本文引用的文献

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The Complexity of Malignant Glioma Treatment.恶性胶质瘤治疗的复杂性
Cancers (Basel). 2025 Mar 4;17(5):879. doi: 10.3390/cancers17050879.
2
A Multi-Omics Analysis of a Mitophagy-Related Signature in Pan-Cancer.泛癌中与线粒体自噬相关特征的多组学分析
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3
Effects of Radiotherapy Alone Versus Concomitant Radiotherapy With Temozolomide Chemotherapy on the Outcome of IDH-wildtype Glioblastoma Patients.单纯放疗与替莫唑胺同步放化疗对异柠檬酸脱氢酶野生型胶质母细胞瘤患者预后的影响。
Clin Oncol (R Coll Radiol). 2025 Feb;38:103741. doi: 10.1016/j.clon.2024.103741. Epub 2024 Dec 19.
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Beta-Caryophyllene Augments Radiotherapy Efficacy in GBM by Modulating Cell Apoptosis and DNA Damage Repair via PPARγ and NF-κB Pathways.β-石竹烯通过PPARγ和NF-κB途径调节细胞凋亡和DNA损伤修复增强胶质母细胞瘤的放疗疗效。
Phytother Res. 2025 Feb;39(2):776-788. doi: 10.1002/ptr.8413. Epub 2024 Dec 13.
5
Cannabigerol (CBG): A Comprehensive Review of Its Molecular Mechanisms and Therapeutic Potential.大麻萜酚(CBG):其分子机制和治疗潜力的全面综述。
Molecules. 2024 Nov 20;29(22):5471. doi: 10.3390/molecules29225471.
6
Structural insight into GPR55 ligand recognition and G-protein coupling.对GPR55配体识别和G蛋白偶联的结构洞察。
Cell Res. 2025 Jan;35(1):76-79. doi: 10.1038/s41422-024-01044-w. Epub 2024 Oct 31.
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Recent Treatment Strategies and Molecular Pathways in Resistance Mechanisms of Antiangiogenic Therapies in Glioblastoma.胶质母细胞瘤抗血管生成疗法耐药机制中的最新治疗策略和分子途径
Cancers (Basel). 2024 Aug 27;16(17):2975. doi: 10.3390/cancers16172975.
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