EC tissues; matching normal esophageal tissues; xenograft tumors; lung tissues
HET-1A; KYSE-150; Eca-109; TE-10; TE-11; 293T; CD8 + T cells
cell line-derived xenograft
ceRNA regulation (other); ERK (promotes); proliferation (promotes); migration (promotes); invasion (promotes); metastasis (promotes); EMT (promotes); apoptosis (promotes); immune regulation (promotes); other pathway/process (other)
RT-qPCR; Clinical Sample Validation; Bioinformatics Analysis; Luciferase Reporter Assay; RIP (RNA Immunoprecipitation); Transfection; CCK8; Colony Formation Assay; Wound Healing Assay; Transwell Assay; Annexin V/PI Flow Cytometry; Flow Cytometry(Non-apoptosis/cycle); Western Blot; In Vivo Animal Model; IHC (Immunohistochemistry); IF (Immunofluorescence); H&E Staining
Higher circ-VIM expression correlated with tumors of advanced TNM stage and positive lymph node metastasis in EC patients.
circ-VIM is up-regulated in esophageal cancer tissues and cell lines, and higher expression is associated with advanced TNM stage and lymph node metastasis. Functionally, circ-VIM promotes EC proliferation, migration, invasion, EMT, metastasis, xenograft growth, and immune escape by sponging miR-124 and derepressing PD-L1, with downstream Ras/ERK signaling involvement. Silencing circ-VIM synergizes with sevoflurane to suppress malignant phenotypes and enhance CD8 + T-cell antitumor activity through the miR-124/PD-L1 axis.
0.7554
CircRNA VIM silence synergizes with sevoflurane to inhibit immune escape and multiple oncogenic activities of esophageal cancer by simultaneously regulating miR-124/PD-L1 axis.
combined biological and clinical study