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

Abstract

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.

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“…On the 28 th day of injection, mice were euthanized by neck dislocation, and the xenografts were harvested, photographed, and weighed. 35 …”

circCCT3 Enhances Invasion and Epithelial-Mesenchymal Transition (EMT) of Non-Small-Cell Lung Cancer (NSCLC) via the miR-107/Wnt/FGF7 Axis

“…Especially, miR-107 could serve as an important downstream effector for lncRNAs or circRNAs in NSCLC [ 3 ]. As for key targets of miR-107, BDNF, CDK6, FGFRL1, and STK33 were confirmed in vitro and in vivo [ 13 , 27 – 29 ]. In our study, we showed Wnt3a was the crucial target of miR-107, which enriched our understanding of how miR-107 inhibited invasion and EMT of NSCLC cells.…”

“…A number of studies revealed that miRNAs regulated tumor proliferation, invasion, and EMT by downstream genes [ 12 ]. miR-107 was recently shown to play a tumor-suppressive role in various cancers, including CRC and NSCLC [ 13 , 14 ].…”

Long Non-Coding RNA NEAT1 Accelerates Lung Cancer Development Via MicroRNA-107/FOXK1 Axis

“…Actually, miR-107 expression demonstrated a decrease in NSCLC, and the augment of miR-107 oppressed the ferocious performance of cancer cells through the modi cation of its downstream actor cyclin-dependent kinase 6 [31]. An experimental exploration has detected that overexpressing miR-107 damaged the malignant phenotype of NSCLC cells partially by serine/threonine kinase 33-meidated extracellular regulated protein kinases pathway [32]. Amazingly, hsa-miR-107, once sponged by lncRNA FYVE, RhoGEF and PH domain containing 5 antisense RNA 1, indirectly offered a niche for NSCLC cells to proliferate [33].…”