Cancer stem cells (CSCs) are closely related to
tumor occurrence, development,
metastasis, drug resistance, and recurrence. The role of CSCs in
melanoma is poorly understood. Our previous studies suggested that the NOP14
nucleolar protein (NOP14) is involved in
melanoma pathogenesis regulation. Importantly, NOP14 overexpression inhibits the Wnt/beta (β)-
catenin signaling pathway, an important mechanism regulating CSCs stemness. Therefore, in this study, we aimed to explore the role of NOP14 in the stemness and function of CSCs in
melanoma in vitro. CD133, a stem cell marker, was used to identify
melanoma stem-like cells (SLCs). NOP14 overexpression subsequently decreased the proportion of CD133+ SLCs, impaired the colony-forming capabilities, and downregulated the expression of Nanog, SOX2, and OCT4 stem cell markers in A375 and A875 cells, suggesting that NOP14 suppresses the stemness of
melanoma SLCs. NOP14 overexpression suppressed the migration, invasion, and angiogenesis-inducing ability of A375-SLCs and A875-SLCs. NOP14 overexpression also inactivated Wnt/β-
catenin signaling in
melanoma CD133+ SLCs. The Wnt signaling activator BML-284 alleviated the effect of NOP14 overexpression on the stemness and function of
melanoma CSCs. In conclusion, NOP14 suppresses the stemness and function of
melanoma SLCs by inactivating Wnt/β-
catenin signaling. Thus, NOP14 is a novel target for CSC treatment in
melanoma.Abbreviations: CSCs, cancer stem cells; SLCs, stem-like cells; NOP14, NOP14
nucleolar protein; SCID,
severe combined immunodeficiency; β-
catenin, beta-
catenin; lv-NOP14, lentivirals expressing NOP14; PBS,
phosphate buffer saline; HUVECs, human umbilical vein endothelial cells.