Abstract

The retinoblastoma (Rb1) gene is one of the most important tumor suppressor genes. Dysfunction of Rb protein drives tumorigenesis by overcoming barriers to cellular proliferation. Consequently, factors modulating Rb function are of great clinical import. Here, we show that miR-26a was differentially expressed in human retinoblastoma cells, tissues and serums from retinoblastoma patients, compared with human retinal microvascular endothelial cells, non-tumor tissues and serums from healthy children, and that it tightly regulated the expression of Rb1 by specifically targeting a conserved sequence motif in its UTR, leading to low expression of Rb1. In vitro experiments determined that miR-26a directly participated in the regulation of cell proliferation of human Y79 RB cells. Our results also suggest that curcumin modulated the miR-26a expression profile, thereby exerting its anti-proliferation effects on Y79 RB cells via up-regulation of Rb1. To our knowledge, these data indicate for the first time that miR-26a directly regulates cell proliferation by targeting Rb1 in retinoblastoma and that miR-26a could be a potential therapeutic approach for retinoblastoma.

Full Text
Published version (Free)

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