Abstract
Cutaneous T-cell lymphoma (CTCL) is associated with the downregulation of miR-337 expression, although the exact underlying mechanism is unknown. In the present work, we investigated the molecular mechanism and function of miR-337 in regulating CTCL cell viability and invasion. We observed that miR-337 expression was downregulated in both CTCL tumors and cell lines. Furthermore, CCK assay, BrdU incorporation assay, and flow cytometry revealed that transfection with the miR-337 mimic resulted in decreased proliferation and increased apoptotic levels in CTCL cells. Results of the Transwell migration assay indicated that the miR-337 mimic decreased CTCL cell invasion in vitro. Both bioinformatics prediction and the dual-luciferase reporter assay revealed that miR-337 targets the 3'-UTR of STAT3 for silencing. Overexpression of STAT3 counteracted the pro-apoptotic influence of miR-337 in CTCL cell lines and restored their invasion properties. The results thus indicate that the miR-337-STAT3 axis inhibits the proliferation of malignant T cells and that miR-337 may serve as a promising therapeutic target for CTCL.