miR-107 inhibited malignant biological behavior of non-small cell lung cancer cells by regulating the STK33/ERK signaling pathway in vivo and vitro

BACKGROUND: The role of miRNAs in non-small cell lung cancer (NSCLC) has been broadly studied and confirmed, and miR-107 has attracted an ever-growing level of attention. This study set out to research the mechanism of the effect of miR-107 on the malignant biological behavior of NSCLC in vivo and vitro. METHODS: The expression of miRNAs related to the development of NSCLC was detected by RT-qPCR. Western blotting was carried out to detect expression levels of serine/threonine kinase 33 (STK33) and proteins related to the extracellular regulated protein kinases (ERK) signaling pathway, while cell proliferation was detected using cell counting kit-8 (CCK-8). The cell apoptosis rate was measured using flow cytometry. The invasion ability was detected by Transwell assay. In vivo tumor growth assays were performed on mice. The expression ERK signaling pathway-related proteins in vivo was evaluated by immunohistochemistry staining. The targeted relationship between miR-107 and STK33 was confirmed by the dual luciferase reporter gene. RESULTS: In NSCLC cell lines and tissues, miR-107 was downregulated. Overexpression of miR-107 inhibited malignant biological behavior of NSCLC cell lines, and suppressed tumor growth in vivo. In addition, STK33 is one of the target genes of miR-107. Therefore, miR-107 suppressed cell proliferation and invasion and promoted tumor growth in vivo and cell apoptosis of NSCLC in vitro. The mechanism was found to be miR-107 targeting STK33, and a lack of STK33 led to the activation of ERK signaling pathway. CONCLUSIONS: miR-107 inhibited malignant biological behavior of NSCLC through regulation of the STK33/ERK signaling pathway.