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Exosomes-derived miR-154-5p attenuates esophageal squamous cell carcinoma progression and angiogenesis by targeting kinesin family member 14.

ABSTRACT: Exosomes participate in the progression and angiogenesis of esophageal squamous cell carcinoma (ESCC). This study aimed to explore the effect and mechanism of exosomes-derived miR-154-5p on the progression and angiogenesis of ESCC. The exosomes with the diameter of 40-270 nm were successfully isolated from ESCC cells by ultracentrifugation. They were then assessed by transmission electron microscope (TEM), nanoparticle tracking analysis (NTA), and Western blotting. Kinesin family member 14 (KIF14) was upregulated, while miR-154-5p was downregulated in ESCC as examined by Quantitative Real-time PCR (qRT-PCR). Exosomes-derived miR-154-5p from ESCC cells was found to attenuate the cellular migration, invasion, and angiogenesis of ESCC using Cell Counting Kit-8 (CCK-8), wound healing assay, transwell migration assay, and tumor formation assays. Moreover, KIF14 was proven to be a direct downstream target gene of miR-154-5p in ESCC cells using luciferase assay. In conclusion, our study identified that exosomes-derived miR-154-5p attenuates ESCC progression and angiogenesis by targeting KIF14 in vitro, which might provide a novel approach for the diagnosis and treatment of ESCC.

SUBMITTER: Shou Y

PROVIDER: S-EPMC8973613 | biostudies-literature | 2022 Feb

REPOSITORIES: biostudies-literature

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Exosomes-derived miR-154-5p attenuates esophageal squamous cell carcinoma progression and angiogenesis by targeting kinesin family member 14.

Shou Yuwei Y Wang Xiaoqian X Liang Yinghao Y Liu Xiaonan X Chen Kuisheng K

Bioengineered 20220201 2

Exosomes participate in the progression and angiogenesis of esophageal squamous cell carcinoma (ESCC). This study aimed to explore the effect and mechanism of exosomes-derived miR-154-5p on the progression and angiogenesis of ESCC. The exosomes with the diameter of 40-270 nm were successfully isolated from ESCC cells by ultracentrifugation. They were then assessed by transmission electron microscope (TEM), nanoparticle tracking analysis (NTA), and Western blotting. Kinesin family member 14 (KIF1 ...[more]

PMID: 35156510

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Project description:BackgroundVascular dementia (VaD) mainly results from cerebral vascular lesions and tissue changes, which contribute to neurodegenerative processes. Effective therapeutic approaches to targeting angiogenesis may reduce mortality of VaD. Endothelial progenitor cells (EPCs) play a key role in postnatal angiogenesis. Many exosomal microRNAs (exo-miRNAs) have been reported to involve in the development of dementia. The present study was designed to investigate whether the expression profile of the exo-miRNAs is significantly altered in patients with VaD and to reveal the function of differentially expressed miRNAs and the relevant mechanisms in EPC-mediated angiogenesis in VaD rat model.ResultsExosomes isolated from serum of patients with VaD (n = 7) and age-matched control subjects (n = 7), and miRNA sequencing and bioinformatics analysis found that circulating exosome miRNA-155-5p, miRNA-154-5p, miR-132-5p, and miR-1294 were upregulated in patients with VaD. The expression of miRNA-154-5p was further verified to be upregulated in clinical samples (n = 23) and 2-vessel occlusion-induced VaD rat model by reverse transcription quantitative PCR (RT-qPCR). Notably, miRNA-154-5p inhibition in bone marrow-EPCs (BM-EPCs) from VaD rats improved EPC functions, including tube formation, migration, and adhesion, and elevated concentrations of vascular endothelial growth factor (VEGF) and stromal cell-derived factor-1α (SDF-1α). The mRNA levels of ICAM-1, VCAM-1, and MCP-1 were reduced in miRNA-154-5p-inhibited EPCs. In addition, miRNA-154-5p inhibition increased the level of superoxide dismutase (SOD), and decreased reactive oxygen species (ROS) in EPCs. PRKAA2 was chosen as a promising target gene of miR-154-5p, and miRNA-154-5p inhibition upregulated the protein expression of AMPKα2. Furthermore, upregulation of miR-154-5p markedly diminished EPC functions and inhibited angiogenesis following EPC transplantation in VaD rats.ConclusionCirculating exo-miR-154-5p was upregulated in patients with VaD, and miR-154-5p upregulation was associated with impaired EPC functions and angiogenesis in VaD rat model. Therefore, miR-154-5p is a promising biomarker and therapeutic strategy for VaD.

Dataset Information

Exosomes-derived miR-154-5p attenuates esophageal squamous cell carcinoma progression and angiogenesis by targeting kinesin family member 14.

Publications

Exosomes-derived miR-154-5p attenuates esophageal squamous cell carcinoma progression and angiogenesis by targeting kinesin family member 14.

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