These results suggest that the three miRNAs are negative regulators of Fus1 expression in lung cancers.

Low DAB2 and high miR-93 expression levels correlate with poor patient survival in non-small cell lung cancer.

miR-29c and miR-429, but not miR-93, may have a role in early stage non-small lung cancer

miR-93/ZNRF3/Wnt/beta-catenin regulatory network contributes to the growth of lung carcinoma.

overexpression of miR-93 in lung cancer cells promoted TGF-b-induced EMT through downregulation of NEDD4L. The analysis of publicly available gene expression array datasets indicates that low NEDD4L expression correlates with poor outcomes among patients with lung cancer, further supporting the oncogenic role of miR-93 in lung tumorigenesis and metastasis.

Data found that miR-93 could target circRNF13, suggesting that circRNF13 might function as an miR-93-5p sponge through the ceRNA mechanism in lung adenocarcinoma.

Both in vivo and in vitro experiments revealed that circCRIM1 suppresses the invasion and metastasis of lung adenocarcinoma (LUAC) by promoting the expression of leukemia inhibitory factor receptor, a well-known tumor suppressor, by sponging miR-93 and miR-182. In the clinical and pathological analyses, the downregulation of circCRIM1 in LUAC was significantly correlated with lymphatic metastasis and TNM stage.

findings demonstrated that cisplatin could effectively inhibit lung adenocarcinoma cell proliferation by decreasing cyclin D2 expression via miR93.

The aim of the study was to assess the levels of expression of interleukin 17A (IL-17A) and microRNA 93 (miRNA-9) in patients with non-small cell lung cancer (NSCLC) in relation to the tumor characteristic (histopathological subtype, cancer stage (TNM and AJCC classification)), and to determine whether correlation between gene IL-17A and miR-9 expression exists.