UNBS5162 inhibits proliferation of human retinoblastoma cells by promoting cell apoptosis

Figures & data

Figure 1 UNBS5162 inhibited cell proliferation of human retinoblastoma cell lines.

Notes: (A, B) Concentration of UNBS5162 treatment was determined by drug sensitivity assay; 16.5 μM was the IC₅₀ value of UNBS5162 treatment. (C, D) Proliferation of WERIRb1 and Y79 examined by CCK8 assay. Compared with the negative-control (NC) group, cell proliferation in the UNBS5162-treated group decreased and showed significant differences at 72 hours in these two cell lines (*P<0.05).

Figure 2 UNBS5162 promoted cell apoptosis of human retinoblastoma cell lines.

Notes: (A, B) Apoptotic cell numbers in negative-control (NC) and UNBS5162-treated groups were examined by flow cytometry. (C, D) Numbers of apoptotic cells in the UNBS5162-treated group (27.1% in WERIRb1, 20.83% in Y79) were significantly higher than in the NC group (11.59% in WERIRb1, 12.89% in Y79; *P<0.05).
Abbreviations: FITC, fluorescein isothiocyanate; PI, propidium iodide.

Figure 3 UNBS5162 affected the expression of apoptosis-related genes in human retinoblastoma cell lines.

Notes: Western blot was used to examine the expression of apoptosis-related genes in the negative-control (NC) and UNBS5162-treated groups. As a result, compared with the NC group, the expression of Caspase 3 p17 and Bax were upregulated and Bcl2 downregulated significantly in WERIRb1 (A) and Y79 (B) cells (*P<0.05).

Figure 4 UNBS5162 inhibited proliferation of human retinoblastoma cells through the Akt–mTOR pathway.

Notes: Following Western blot, expression of Akt-pathway and key proliferation-related genes – those for p-Akt, p-mTOR, p70, and cyclin D₁ – was found to be downregulated significantly in the UNBS5162-treated group compared with the negative-control (NC) group in WERIRb1 (A) and Y79 (B) cells (*P<0.05).