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Aberrantly expressed miR-582-3p maintains lung cancer stem cell-like traits by activating Wnt/?-catenin signalling.

ABSTRACT: Cancer stem cells (CSCs) are involved in tumorigenesis, tumour recurrence and therapy resistance and Wnt signalling is essential for the development of the biological traits of CSCs. In non-small cell lung carcinoma (NSCLC), unlike in colon cancer, mutations in ?-catenin and APC genes are uncommon; thus, the mechanism underlying the constitutive activation of Wnt signalling in NSCLC remains unclear. Here we report that miR-582-3p expression correlates with the overall- and recurrence-free-survival of NSCLC patients, and miR-582-3p has an activating effect on Wnt/?-catenin signalling. miR-582-3p overexpression simultaneously targets multiple negative regulators of the Wnt/?-catenin pathway, namely, AXIN2, DKK3 and SFRP1. Consequently, miR-582-3p promotes CSC traits of NSCLC cells in vitro and tumorigenesis and tumour recurrence in vivo. Antagonizing miR-582-3p potently inhibits tumour initiation and progression in xenografted animal models. These findings suggest that miR-582-3p mediates the constitutive activation of Wnt/?-catenin signalling, likely serving as a potential therapeutic target for NSCLC.

PROVIDER: S-EPMC4667703 | BioStudies |

REPOSITORIES: biostudies

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