Aims
To determine the functional role of miR-509-3p in melanoma. Study design: Cell culture study.
Background
microRNAs (miRNAs) are ubiquitously dysregulated in numerous tumor cell types, including melanoma cells. The anti-tumor effect of miR-509-3p was widely evaluated in various cancers. Aims: To determine the functional role of miR-509-3p in melanoma. Study design: Cell culture study.
Conclusion
miR-509-3p suppressed the biological function of melanoma cells through negatively regulating CTHRC1, shedding light on miR-509-3p as a potential candidate for melanoma therapeutics and treatments.
Methods
Expression of miR-509-3p in melanoma cell models were assessed by qRT-PCR. Cell migration and invasion were analyzed by wound healing and transwell assays, respectively. Expression levels of biomarkers of epithelial-mesenchymal transition were determined by Western blot. Luciferase vectors containing wildtype or mutant miR- 509-3p binding site were constructed, and then dual-luciferase reporter assay.
Results
Dysregulated miR-509-3p level was found in melanoma cells. Elevated miR-509-3p expression suppressed melanoma cell migration (P < .001) and invasion (P < .001) capacities. Epithelial-mesenchymal transition of melanoma cells was repressed by miR-509-3p, along with increased α-catenin/E-cadherin (P < .001) and decreased vimentin/ fibronectin (P < .001). CTHRC1 (collagen triple helix repeat containing 1) contained a potential binding site for miR-509-3p, and miR- 509-3p decreased protein expression of CTHRC1 in melanoma cells (P < .001). CTHRC1 promoted melanoma cell migration and invasion (P < .001), as well as contributed to epithelial-mesenchymal transition. Increased CTHRC1 expression attenuated miR-509-3p-induced inhibition of melanoma cell migration (P < .001), invasion, and epithelial- mesenchymal transition.