Abstract: Objective To investigate the effect of sennoside B on proliferation, apoptosis, invasion and Wnt / β-catenin signaling pathway of retinoblastoma HXO-Rb44 cells. Methods HXORB44 cells were treated with different doses (0, 5, 10 and 20 μmol / L) of sennoside B, and the cells were randomly divided into four groups: Control group, sennoside B 5 μmol / L group, sennoside B 10 μmol / L group and sennoside B 20 μmol / L group. Cell viability was detected by MTT assay. Colony formation assay was used to detect the colony formation rate. Cell apoptosis rate was detected by flow cytometry. Cell invasion were detected by Transwell assay. Cell pellet-forming experiment was used to detect the diameters and numbers of cell pellets. The protein expression levels of Cleaved Caspase-3, Caspase-3, MMP-2, MMP-9, SOX2, OCT4, CD44, Wnt1, β-cateninwere detected by Western blotting. Results The cell viabilities and colony formation rates in thesennoside B 10 and 20 μmol / L groups were significantly decreased when compared with those in theControl group ( P < 0. 05), the cell apoptosis rates and cleaved Caspase-3 / Caspase-3 expression levels were significantly increased when compared with those in the Control group (P < 0. 05). Thenumbers of invaded cells and the protein expression levels of MMP-2 and MMP-9 were significantlydecreased in the sennoside B 10 and 20 μmol / L groups (P < 0. 05), the cell pellet diameters, thecell pellet numbers and the protein expression levels of SOX2, OCT4 and CD44 were significantly decreased (P< 0. 05), and the protein expression levels of Wnt1 and β-catenin were significantlydecreased in the sennoside B 10 and 20 μmol / L groups when compared with those in the Controlgroup (P< 0. 05). Conclusion Sennoside B can induce apoptosis, inhibit the proliferation, invasion and stem-like characteristics of retinoblastoma HXO-Rb44 cells, and inhibit the activation of Wnt / β-catenin signaling pathway.

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