DUSP1 promotes senescence of retinoblastoma cell line SO-Rb5 cells by activating AKT signaling pathway

C.-M. Cheng, F. Liu, J.-Y. Li, Q.-Y. Song

Department of Ophthalmology, Mudanjiang Medical University Hongqi Hosptial, Mudanjiang, Heilongjiang, China. r4q7kr7l488h@sina.com

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• Oncology

OBJECTIVE: Retinoblastoma seriously threats to human health and life. Molecular targeted therapy of retinoblastoma supplies the direction of research in the future. This study aims to investigate the impact of DUSP1 on human retinoblastoma SO-Rb5 cell senescence.

MATERIALS AND METHODS: Angiotensin II (AGII) was used to induce human retinoblastoma SO-Rb5 cell senescence model. DUSP1 over-expression plasmid and small interfere RNA (siRNA) were transfected into SO-Rb5 cells by Lipofectamine. Dual specificity phosphatase 1 (DUSP1), p53, p16, and protein kinase B (Akt) signaling expressions were detected with Western blot assay. SH-6 was applied to inhibit Akt signaling in SO-Rb5 cells. Cell senescence was evaluated by using β-galactosidase test.

RESULTS: DUSP1 level increased in SO-Rb5 cells induced by AGII. Senescence protein p53 and p16 significantly upregulated in SO-Rb5 cell senescence model, together with β-galactosidase staining. DUSP1 plasmid transfection significantly enhanced DUSP expression, triggered SO-Rb5 cell senescence, and inhibited Akt signaling activation. DUSP1 siRNA exhibited the opposite effects. SH-6 significantly increased SO-Rb5 cell senescence induced by AGII through inhibiting Akt signaling.

CONCLUSIONS: DUSP1 facilitated human retinoblastoma SO-Rb5 cell senescence induced by AGII through inhibiting Akt signaling pathway.

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