Publication Date
1-1-2021
Journal
Technology in Cancer Research & Treatment
Abstract
Lung cancer is listed as the most common reason for cancer-related death all over the world despite diagnostic improvements and the development of chemotherapy and targeted therapies. MicroRNAs control both physiological and pathological processes including development and cancer. A microRNA-9 to 1 (miR-9 to 1) overexpression model in lung cancer cell lines was established and miR-9 to 1 was found to significantly suppress the proliferation rate in lung cancer cell lines, colony formation in vitro, and tumorigenicity in nude mice of A549 cells. Ubiquitin-like containing PHD and RING finger domains 1 (UHRF1) was then identified to direct target of miR-9 to 1. The inhibition of UHRF1 by miR-9 to 1 causes G1 arrest and p15, p16, and p21 were re-expressed in miR-9 to 1 group in mRNA level and protein level. Silence of UHRF1 expression in A549 cells resulted in the similar re-expression of p15, p16, p21 which is similar with miR-9 to 1 infection. Therefore, we concluded that UHRF1 is a new target for miR-9 to 1 to suppress cell proliferation by re-expression of tumor suppressors p15, p16, and p21 mediated by UHRF1.
Keywords
Adult, Aged, Animals, Apoptosis, CCAAT-Enhancer-Binding Proteins, Cell Line, Tumor, Cell Movement, Cell Proliferation, Computational Biology, Disease Models, Animal, Female, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Genes, Reporter, Heterografts, Humans, Lung Neoplasms, Male, Mice, MicroRNAs, Middle Aged, RNA Interference, Transcriptome, Ubiquitin-Protein Ligases