High expression of miR5700 in atypical type A thymoma and its role in promoting tumour progression

Abstract Objective Relapse and lung metastasis of atypical type A thymoma are knotty problems in clinical treatment. The identification of specific biomarkers and novel therapeutic targets is critical for advancing the precision and efficacy of interventions against this disease. MicroRNAs (miRNAs), as pivotal regulators of gene expression, have emerged as key players in tumorigenesis and metastatic processes. In this study, we found that miR5700 was overexpressed in atypical type A thymoma, and miR5700 overexpression could promote lung cancer cell proliferation, migration, and invasion abilities. It gives us a clue that miR5700 could be a biomarker and therapeutic target for atypical type A thymoma. Methods miRNA microarray chip technology was applied to identify differentially expressed miRNAs in 20 pairs of atypical type A thymoma versus type A thymoma. Real‐time reverse transcriptase‐polymerase chain reaction (RT‐PCR) was performed to detect the expression of miR5700 in non‐small cell lung cancer cells after lentiviral transfection. Subsequently, cell proliferation was examined by the real‐time cellular analysis and clone formation assay. Cell migration and invasion abilities were evaluated by wound healing and Matrigel transwell assay, respectively. Besides, the effect of miR5700 on AKT, mTOR, and β‐catenin was determined by western blotting. Results MiR5700 was dramatically increased in atypical A thymoma. The transfection of miR5700 into A549 and H2170 cells significantly promoted cell growth, migration, and invasion. Furthermore, miR5700 was confirmed to upregulate the expression of AKT, mTOR and β‐catenin proteins, which were related to tumour progression by western blotting. Conclusions High expression of miR5700 is a new hallmark that could promote tumour progression. Additionally, it is hoped that miR5700 will become a potential target for the diagnosis of atypical type A thymoma through further research in the future.