<p>MiR-216b suppresses cell proliferation, migration, invasion, and epithelial&ndash;mesenchymal transition by regulating FOXM1 expression in human non-small cell lung cancer</p>

Abstract

Background/aims: MiR-216b and forkhead box M1 (FOXM1) were demonstrated to exert their biological effects on the development and progression of tumors. This study aimed to investigate the expression and role of miR-216b and FOXM1 in tissues and cell lines of non-small cell lung cancer (NSCLC). Methods: The expressions of miR-216b and FOXM1 in NSCLC tissues and cells were detected by qRT-PCR and Western blot analysis. Cell proliferation was measured by CCK-8 assay. Cell migration and invasion were confirmed by Transwell assay. Finally, the bioinformatics and dual-luciferase reporter assay were conducted to validate the relationship of miR-216b and FOXM1. Results: Compared with normal tissues and cells, the expression of miR-216b was obviously decreased in NSCLC tissues and cells. However, the expressions of FOXM1 mRNA and protein were significantly increased, and negatively correlated with the expression of miR-216b. Multivariate Cox’s regression analysis suggested that miR-216b or FOXM1 expression was an independent prognostic factor for patients with NSCLC. MiR-216b overexpression remarkably repressed cell proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT) of NSCLC cells. The bioinformatics and dual-luciferase reporter assay validated that the 3ʹ-untranslated region (3ʹ-UTR) of FOXM1 mRNA was indeed a direct target of FOXM1. In vitro, overexpression of FOXM1 partially eliminated inhibitory effects of miR-216b on cell proliferation, migration, and invasion, whereas inhibition of FOXM1 contributed to inhibitory effects mediated by miR-216b. Conclusion: MiR-216b inhibits cell proliferation, migration, invasion, and EMT by targeting the expression of FOXM1 in human NSCLC. These findings suggested a potential therapeutic role of miR-216b in patients of NSCLC.

Differential Expression of miRNAs in Hypoxia (“HypoxamiRs”) in Three Canine High-Grade Glioma Cell Lines

“…In this same study, the authors identify forkhead box protein M1 (FOXM1) as a direct target, and ectopic expression of miR-216b led to a decrease in FOXM1 protein levels and percentage of Ki-67-positive cells in xenograft models. A similar mechanism has been shown for melanoma (99), hepatocellular carcinoma (100), non-small-cell lung carcinoma (101), and osteosarcoma (102), and low miR-216b levels in tumors are independent poor prognostic indicators in many of these cancers. In pancreatic cancer, this miRNA functions in a tumor-suppressive way by targeting translationally controlled tumor protein (TPT1), and levels of this miRNA are significantly associated with large tumor size and advanced TNM stage (103).…”

Thiostrepton and miR‑216b synergistically promote osteosarcoma cell cytotoxicity and apoptosis by targeting FoxM1

“…miR-216b is downregulated in non-small cell lung cancer (NSCLC) tissues and cell lines. Multivariate Cox regression analysis indicated that miR-216b is an independent prognostic factor for patients with NSCLC (39). By targeting FoxM1 and SOX9, miR-216b regulates NSCLC proliferation and invasion (39,40).…”

“…Multivariate Cox regression analysis indicated that miR-216b is an independent prognostic factor for patients with NSCLC (39). By targeting FoxM1 and SOX9, miR-216b regulates NSCLC proliferation and invasion (39,40). miR-216b is also downregulated in breast cancer samples, which suppresses breast cancer cell proliferation by targeting the purinergic receptor P2X7 (41).…”

Soy isoflavone genistein inhibits hsa_circ_0031250/miR‐873‐5p/FOXM1 axis to suppress non‐small‐cell lung cancer progression

“…46 Furthermore, the reports of Yuan et al and Wang et al indicated that FOXM1 could promote cell proliferation, migration and invasion in NSCLC cells. 47,48 These all suggested the carcinogenic role of FOXM1 in NSCLC. Similarly, our study also found this function, and identified that miR-873-5p constrained NSCLC cell progression under genistein exposure by decreasing FOXM1.…”