Anillin(ANLN) promoting melanoma malignant progression via miR-200b-3p/ANLN/CDK1/p53 signaling axis

Abstract Background Melanoma is a highly malignant tumor originating from melanocytes, characterized by its aggressive invasion, metastasis, and poor prognosis. Anillin (ANLN), a multi-domain protein, plays a crucial role in cell division. Evidence suggests that abnormal ANLN expression leads to irregular cell division, promoting tumor proliferation, migration, and invasion. However, its role in melanoma remains unexplored. Methods Bioinformatics, quantitative PCR, and Western blot were employed to detect ANLN mRNA and protein expression levels in both normal and cancer cells. The dual-luciferase reporter assay was utilized to identify the interaction between ANLN and the upstream target microRNA. The invasion and metastasis of A875 and SK-MEL-28 cells were examined using Transwell assays. Flow cytometry was employed to analyze cell cycle and apoptosis. The role of ANLN in the initiation and development of melanoma was further assessed in a mouse model. Results ANLN was highly expressed in melanoma samples and cells. Biofunctional assays confirmed that ANLN promoted the proliferation, invasion, and metastasis of melanoma cells in vitro in nude mice. The dual-luciferase report revealed that the upstream target microRNA of ANLN, miR-200b-3p, negatively regulated ANLN expression and influenced the malignant progression of melanoma. Protein-protein interaction analysis suggested that ANLN might positively regulate CDK1 expression and impact the P53 signaling pathway, modulating melanoma proliferation, migration, and invasion. Conclusion ANLN is associated with the malignant progression of melanoma and regulates the melanoma cell cycle through the miR-200b-3p/ANLN/CDK1 axis. This interaction further influences the P53 signaling pathway, promoting melanoma development and progression.