MiR‐21 inhibitor suppressed the progression of retinoblastoma via the modulation of PTEN/PI3K/AKT pathway. (27th September 2016)

• Record Type: Journal Article
• Authors: Gui, Fu; Hong, Zhengdong; You, Zhipeng; Wu, Hongxi; Zhang, Yulan
• Is Part Of: Cell biology international. Volume 40:Number 12(2016)
• Page Start: 1294
• Page End: 1302
• Publication Date: 2016-09-27
• Subjects: invasion -- migration -- miRNA‐21 -- proliferation -- PTEN/PI3K/AKT signal -- retinoblastoma; Cytology -- Periodicals; Cells -- Periodicals; 571.605
• DOI: 10.1002/cbin.10678
• Languages: English
• ISSNs: 1065-6995

Abstract

Abstract: MicroRNA‐21 (miR‐21) was reported to act as an oncogene during the development of many human tumors. However, little was revealed about the function of miR‐21 in retinoblastoma (RB). In this study, we examined the expression of miR‐21 in RB tissues and explored the relationship between miR‐21 and phosphatase and tensin homolog (PTEN)/phosphatidylinositol‐3‐OH kinase (PI3K)/AKT signal. Quantitative real‐time PCR (qRT‐PCR) results showed that the level of miR‐21 in RB tissues was higher than that in retinal normal tissues. In Weri‐Rb‐1 cells, miR‐21 inhibitor suppressed the expression of miR‐21 and cell viability, but improved cell apoptotic rates by modulating the levels of PDCD4, Bax, and Bcl‐2. Meanwhile, miR‐21 inhibitor suppressed cell migration and invasion via inhibiting the protein levels of MMP2 and MMP9 and significantly affected the expression of PTEN, PI3K, and p‐AKT. Taken together, miR‐21 inhibitor suppressed cell proliferation, migration, and invasion via the PTEN/PI3K/AKT signal. These findings revealed the molecular basis of miR‐21 functioning in the progression of RB and provided a new means for cell therapy in RB.