BANCR contributes to the growth and invasion of melanoma by functioning as a competing endogenous RNA to upregulate Notch2 expression by sponging miR‑204

Abstract

BRAF-activated non-coding RNA (BANCR) is a long non-coding RNA (lncRNA) that contributes to the initiation and development of many solid tumors, including melanoma. However, the BANCR functions and downstream mechanisms are largely unknown. In this study, we aim to investigate how BANCR participates in the proliferation and migration of malignant melanoma and elucidate the underlying mechanism in this process. We found that the expression of the BANCR was low in melanocytic nevus and human melanocytes but high in melanoma tissues and cell lines. Knockdown of BANCR inhibited melanoma cell proliferation and invasion, and induced cell apoptosis. The decreased expression of relative marker proteins further demonstrated the inhibitory effect of BANCR siRNA in cell growth and migration. Then, we detected downregulation of microRNA-204 (miR‑204), a suppressor of melanoma growth, in melanoma tissues and cell lines. We identified that miR‑204 was a direct target of BANCR and neurogenic locus notch homolog protein 2 (Notch2) was a direct target of miR‑204. BANCR may promote melanoma cell growth through inhibition of miR‑204, leading to the activation of Notch2 pathway. By tumorigenicity assay in BALB/c nude mice, we further demonstrated that BANCR knockdown inhibited tumor growth in vivo. Our results suggest the BANCR/miR‑204/Notch2 axis mediates melanoma cell proliferation and tumor progression.