Mitochondrion-Directed Nanoparticles Loaded with a Natural Compound and a microRNA for Promoting Cancer Cell Death via the Modulation of Tumor Metabolism and Mitochondrial Dynamics.
Yu-Li LoChen-Shen WangYen-Chun ChenTse-Yuan WangYih-Hsin ChangChun-Jung ChenChing-Ping YangPublished in: Pharmaceutics (2020)
Mitochondrial dysfunction may cause cancer and metabolic syndrome. Ellagic acid (abbreviated as E), a phytochemical, possesses anticancer activity. MicroRNA 125 (miR-125) may regulate metabolism. However, E has low aqueous solubility, and miR-125 is unstable in a biological fluid. Hence, this study aimed to develop nanoparticle formulations for the co-treatment of miR-125 and E. These nanoparticles were modified with one mitochondrion-directed peptide and a tumor-targeted ligand, and their modulating effects on mitochondrial dysfunction, antitumor efficacy, and safety in head and neck cancer (HNC) were evaluated. Results revealed that miR-125- and E-loaded nanoparticles effectively targeted cancer cells and intracellular mitochondria. The co-treatment significantly altered cellular bioenergetics, lipid, and glucose metabolism in human tongue squamous carcinoma SAS cells. This combination therapy also regulated protein expression associated with bioenergenesis and mitochondrial dynamics. These formulations also modulated multiple pathways of tumor metabolism, apoptosis, resistance, and metastasis in SAS cells. In vivo mouse experiments showed that the combined treatment of miR-125 and E nanoparticles exhibited significant hypoglycemic and hypolipidemic effects. The combinatorial therapy of E and miR-125 nanoparticles effectively reduced SAS tumor growth. To our best knowledge, this prospective study provided a basis for combining miRNA with a natural compound in nanoformulations to regulate mitochondrial dysfunction and energy metabolism associated with cancer.
Keyphrases
- cell proliferation
- long non coding rna
- combination therapy
- cell death
- cell cycle arrest
- long noncoding rna
- papillary thyroid
- metabolic syndrome
- induced apoptosis
- oxidative stress
- drug delivery
- squamous cell
- healthcare
- pi k akt
- transcription factor
- squamous cell carcinoma
- signaling pathway
- stem cells
- adipose tissue
- low grade
- cell therapy
- replacement therapy
- ionic liquid
- fatty acid
- pluripotent stem cells