LINC01116 promotes nascent protein synthesis and cellular stemness through the miR-432-5p/FKBP7/14 regulatory axis in melanoma.

Skin cutaneous melanoma (SKCM) is a highly aggressive and malignant neoplasm. A wealth of evidence highlights the critical role of LINC01116 in tumorigenesis and progression. Additionally, numerous small molecules within the FK506-binding protein (FKBP) family have been implicated in cancer development. Herein, we interrogated the functional significance of lncRNA LINC01116 and FKBP7/14 in melanoma pathogenesis. This study aim to the expression of long non-coding RNA (lncRNA) LINC01116 in melanoma and its mechanistic role in promoting de novo protein synthesis and cancer stemness through the miR-432-5p/FKBP7/14 axis. A competing endogenous RNA (ceRNA) network for LINC01116 was constructed through bioinformatics analysis. LINC01116 expression levels were assessed in clinical melanoma tissues, adjacent normal tissues, and melanoma cell lines. In vitro experiments included dual-luciferase reporter assays to validate miR-432-5p targeting of FKBP7/14, quantitative PCR (qPCR) and western blotting (WB) to quantify gene/protein expression, and sphere-forming assays to assess protein synthetic capacity and stemness. In vivo, xenograft mouse models were employed to evaluate tumor growth. LINC01116 was significantly upregulated in melanoma tissues and correlated with adverse clinical outcomes. Overexpression of LINC01116 enhanced melanoma cell proliferation, spheroid formation, and invasive potential in vitro. Mechanistically, LINC01116 acted as a sponge for miR-432-5p, thereby upregulating FKBP7/14. In vivo, LINC01116 overexpression accelerated tumor growth in xenograft models. Our findings unveil a novel LINC01116/miR-432-5p/FKBP7/14 axis that drives melanoma stemness and protein synthesis addiction. These insights identify promising therapeutic targets for melanoma intervention.