Aim of the studyThis study aimed to observe the expressions of heat shock protein 27 (HSP27) and proliferating cell nuclear antigen (PCNA) in retinoblastoma (Rb) cells and to explore the relationships of the expression with Rb differentiation and optic nerve infiltration.Material and methodsHeat shock protein 27 and PCNA expressions in 36 routine Rb paraffin specimens were observed using PV9000 two-stage immunohistochemical staining. The correlations of the HSP27 and PCNA expressions with Rb differentiation and optic nerve infiltration were analyzed.ResultsHeat shock protein 27 was weakly expressed in the normal retina, specifically in the ganglion cell layer. It was extensively expressed in Rb tissues at a positive rate of 69.4%, and the positive substances were primarily located in the cytoplasm. Proliferating cell nuclear antigen was expressed weakly or not at all expressed in the normal retina and was extensively expressed in Rb tissues at a positive rate of 83.3%, and the positive substances were primarily located in the nucleus. The positive expression rates of HSP27 and PCNA in the differentiated group were significantly higher than in the undifferentiated group (p < 0.05). The positive expression rates of HSP27 and PCNA in the optic nerve-infiltrated group were significantly higher than in the non-infiltrated group (p < 0.05). Heat shock protein 27 expression was positively correlated with PCNA expression in Rb (p < 0.01).ConclusionsHeat shock protein 27 and PCNA expressions are markedly correlated with cell differentiation and optic nerve infiltration in Rb.

This study aimed to investigate the effect of bruceine D on the proliferation and apoptosis of human retinoblastoma cells and its effect on miR-155 expression. Y79 human retinoblastoma cells were cultured in vitro and randomly divided into the blank control group, DMSO (Dimethyl Sulphoxide) group, bruceine D 10 μmol/L group, bruceine D 20 μmol/L group, and bruceine D 40 μmol/L group. MTT assay was used to detect cell hyperplasia, flow cytometry to detect the apoptosis rate, and qRT-PCR to detect the expression level of miR-155. Anti-miR-155 or miR-155 mimics were transfected into Y79 cells, and hyperplasia and apoptosis rates were detected by the above methods. Western blotting was used to detect Bcl-2, Bax, and caspase-3 expression. Bruceine D can reduce the viability of Y79 cells (P < 0.05), significantly increase the apoptosis rate (P < 0.05), promote the expression of Bax and caspase-3 (P < 0.05), and inhibit miR-155 and Bcl-2 (P < 0.05). Compared with the anti-miR-con group, in the anti-miR-155 group, cell vigor was evidently reduced (P < 0.05), the apoptosis rate was evidently increased (P < 0.05), and the Bcl-2 level was reduced (P < 0.05). Bax and caspase-3 levels were evidently increased (P < 0.05). Transfection with miR-155 mimics can reduce the influence of caspase D-3 in hyperplasia and apoptosis of Y79 cells. Bruceine D may reduce the hyperplasia of human retinoblastoma cells and regulate cell apoptosis by downregulating miR-155 expression.