Uncovering the oncogenic role of RTTN in melanoma pathogenesis and its therapeutic implications.

backgroundSkin cancer, particularly melanoma—an aggressive malignancy originating from melanocytes—poses a significant global health challenge due to its rising incidence and high mortality. Despite advances in understanding melanoma pathogenesis, the role of the RTTN gene, also known as Rotatin, which regulates cell cycle progression, cytoskeletal dynamics, and proliferation, remains largely unexplored in this context. While RTTN has been implicated in other cancers, its function in melanoma progression and potential therapeutic relevance remains unclear. METHODS AND

resultsIn this study, we investigated RTTN’s role in melanoma through a series of in vitro and in vivo experiments. Our analysis revealed that RTTN is significantly upregulated in melanoma tissues and cell lines compared to normal controls through quantitative real-time PCR and Western blotting, and its elevated expression correlates with poor patient prognosis. Functional studies demonstrated that RTTN knockdown suppresses melanoma cell proliferation (assessed by CCK-8 assay), migration (via wound healing assay), and invasion (using Transwell assay).A xenograft mouse model was established using stable RTTN-knockdown cells for in vivo validation, which confirmed that RTTN depletion inhibits tumor growth. Moreover, an experimental lung metastasis model demonstrated that RTTN knockdown significantly impairs the metastatic capacity of melanoma cells.

conclusionsThese findings collectively suggest that RTTN acts as an oncogenic driver in melanoma progression, highlighting its potential as a prognostic biomarker and therapeutic target. This study provides novel insights into the molecular mechanisms of melanoma and underscores the need for further exploration of RTTN in cancer biology.