LINC01116 Facilitates Melanoma 1 Progression Via Sequestering miR-3612 and Up-regulating GDF11 and SDC3

Melanoma is the deadliest cutaneous malignant tumor with high risks. Though increasing evidence has widely referred to the involvement of long non-coding RNAs (lncRNAs) in the mechanism of tumor development, including melanoma, the functional roles of most lncRNAs in melanoma remain to be explored. In this study, we focus on disclosing the role of long intergenic non-protein coding RNA 1116 (LINC01116) in melanoma.

Firstly, we detected LINC01116 expression through RT-qPCR. Functional analysis and animal experiments were carried out to assess the role of LINC01116 in vivo and in vitro. Western blot analysis was employed for detection of important markers regarding epithelial mesenchymal transition (EMT). In addition, RNA pulls down, RIP and luciferase reporter assays were performed to probe into the regulatory mechanism of LINC01116.

LINC01116 was significantly up regulated in melanoma cells. LINC01116 deficiency abrogated cell proliferation, migration, invasion and EMT in melanoma. Moreover, LINC01116 enhanced growth differentiation factor 11 (GDF11) and syndecan 3 (SDC3) expression through sponging microRNA-3612 (miR-3612). The oncogenic role of the LINC01116/miR-3612/GDF11/SDC3 axis in melanoma was finally demonstrated.

Conclusively, LINC01116 sequestered miR-3612 and targeted GDF11 and SDC3 to contribute to the progression of melanoma.