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Esophageal squamous cell carcinoma (ESCC) is a malignancy of the alimentary tract resulting in death worldwide. The role and underlying mechanism of hsa-miR-1269a in the progression of ESCC remain unclear. In this study, hsa-miR-1269a was screened by differential expression analysis in TCGA, and its target gene FAM46C was predicted. qRT-PCR was conducted to assay the expression of hsa-miR-1269a and FAM46C in ESCC cells. The results showed that hsa-miR-1269a was upregulated in ESCC tissues and cell lines. Hsa-miR-1269a overexpression stimulated the proliferation, migration, and invasion capacities of ESCC cells, and FAM46C overexpression inhibited these phenotypes. Dual-luciferase assay verified that hsa-miR-1269a could target FAM46C. Next, qRT-PCR and western blot demonstrated that hsa-miR-1269a overexpression downregulated FAM46C. Rescue experiments revealed that hsa-miR-1269a accelerated the malignant progression of ESCC through FAM46C down-regulation. These results indicate that the interaction between hsa-miR-1269a and FAM46C plays a regulatory role in driving the malignant progression of ESCC cells, thereby providing a novel molecular mechanism for understanding ESCC. • MiR-1269a was up-regulated while FAM46C was down-regulated in esophageal cancer. • MiR-1269a facilitated cell proliferation, migration, invasion, and restrained cell apoptosis of esophageal cancer. • MiR-1269a suppressed FAM46C in esophageal cancer. • MiR-1269a exacerbated progression of esophageal cancer via targeting FAM46C. [ABSTRACT FROM AUTHOR]

Dysregulation of microRNA (miRNA) expression is a critical event in the development and progression of non-small-cell lung cancer (NSCLC). miR-384 has been identified as a novel cancer-related miRNA in numerous cancers, but little is known about its role and functional mechanism in NSCLC. In this study, we found that miR-384 was significantly downregulated in NSCLC tissues and cell lines. The overexpression of miR-384 repressed the growth and invasion of NSCLC cells, whereas its suppression showed the opposite effect. Moreover, astrocyte elevated gene-1 (AEG-1) was identified as a target gene of miR-384. The overexpression of miR-384 significantly decreased AEG-1 expression and Wnt signaling, whereas its suppression promoted this pathway. Furthermore, miR-384 was inversely correlated with AEG-1 expression in NSCLC tissues. Additionally, restoration of AEG-1 expression in miR-384-overexpressing cells significantly reversed the antitumor effects of miR-384. Taken together, these results reveal that miR-384 represses the growth and invasion of NSCLC cells by targeting AEG-1. Our study suggest that miR-384 and AEG-1 may serve as potential targets for the diagnosis and treatment of NSCLC. [ABSTRACT FROM AUTHOR]

N-myc downstream-regulated gene 2 (NDRG2) has been recognised as a negative regulator of the progression of numerous tumours, yet its specific role in small-cell lung carcinoma (SCLC) is not fully understood. The purpose of the current study was to investigate the biological role and mechanism of NDRG2 in SCLC. Initial investigation using the Gene Expression Omnibus (GEO) dataset revealed marked downregulation of NDRG2 transcripts in SCLC. The decreased abundance of NDRG2 in SCLC was verified by examining clinical specimens. Increasing NDRG2 expression in SCLC cell lines caused significant changes in cell proliferation, cell cycle progression, colony formation, and chemosensitivity. NDRG2 overexpression decreased the levels of phosphorylated PTEN, AKT and mTOR. In PTEN-depleted SCLC cells, the upregulation of NDRG2 did not result in any noticeable impact on AKT or mTOR activation. Additionally, the reactivation of AKT reversed the antitumour effects of NDRG2 in SCLC cells. Notably, increasing NDRG2 expression retarded the growth of SCLC cell-derived xenografts in vivo. In conclusion, NDRG2 serves as an inhibitor of SCLC, and its cancer-inhibiting effects are achieved through the suppression of AKT/mTOR via the activation of PTEN. This work suggests that NDRG2 is a potential druggable target for SCLC treatment. [Display omitted] • The overexpression of NDRG2 exhibited tumour-suppressive effects on SCLC. • The overexpression of NDRG2 reduced the phosphorylation of PTEN, AKT, and mTOR. • NDRG2 regulated the activation of AKT and mTOR through PTEN. • NDRG2 interfered with the progression of SCLC through the PTEN-mediated AKT/mTOR pathway. [ABSTRACT FROM AUTHOR]