Abstract

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.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.