Ligusticum chuanxiong Hort. Targets hsa-miR-10a-5p to Potentially Induce Apoptosis and Modulate Lipid Metabolism in Glioblastoma: A Natural-Product-Based Therapeutic Strategy

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Detalles Bibliográficos
Publicado en:	Pharmaceuticals vol. 18, no. 10 (2025), p. 1553-1579
Autor principal:	Xiao-Xuan, Cai
Otros Autores:	Hua-Li, Zuo, Li, Jing, Hsi-Yuan, Huang, Li-Ping, Li, Ni Jie, Pei-Sen, Wu, Xiao-Yuan, Xu, Zhang, Dan, Yue-Yang, Xie, Huang Hsien-Da, Yang-Chi-Dung, Lin
Publicado:	MDPI AG
Materias:	Medical prognosis Metastasis Collagen Spectrum analysis Glioma Traditional Chinese medicine Extracellular matrix MicroRNAs Metabolism Lipids Genes Apoptosis Cell growth Metabolites Morphology Survival analysis Chemotherapy Drug dosages
Acceso en línea:	Citation/Abstract Full Text + Graphics Full Text - PDF
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Descripción
Resumen:	Background/Objectives: Glioblastoma (GBM), the most aggressive primary malignant brain tumor, has a dismal prognosis and limited treatment options. The dried rhizome of Ligusticum chuanxiong Hort. (Chuanxiong, CX) is a traditional Chinese medicinal herb frequently prescribed in formulas intended to invigorate blood circulation. CX also exhibits anti-glioma activity, but its molecular mechanisms remain incompletely understood. Methods: In this study, we combined transcriptomics and Raman spectroscopy to investigate the effects of reconstituted CX-dispensing granules (hereafter referred to as CXG solution) on U87MG cells, suggesting their dual role in promoting cell death and modulating collagen deposition and lipid metabolism. Results: Mechanistically, we demonstrated that the CXG solution downregulates hsa-miR-10a-5p, which directly targets BCL2L11, known to induce pro-apoptotic effects, as validated by qPCR and dual-luciferase reporter assays. Furthermore, the CXG solution and hsa-miR-10a-5p suppress lipid metabolism through a coherent feed-forward loop via targeting transcription factors SREBF1 and E2F1. An electrophoretic mobility shift assay (EMSA) confirmed E2F1 binds to the hsa-miR-29a promoter, leading to the synergistic repression of hsa-miR-29a-3p by SREBF1 and E2F1. Network pharmacology analysis combined with molecular docking suggested that the ferulic acid and adenosine in CX potentially modulate EGFR-the E2F1-hsa-miR-10a-5p axis. Conclusions: These findings elucidate CX’s multi-target anti-GBM mechanisms and propose a novel therapeutic strategy combining metabolic intervention with miRNA-targeted therapy, providing novel insights into feed-forward loop regulation in miRNA networks.
ISSN:	1424-8247
DOI:	10.3390/ph18101553
Fuente:	Research Library