Abstract
Numerous reports have indicated that microRNA‑93‑5p (miR‑93‑5p) is involved in the development and progression of human cancer, including non‑small cell lung, gastric and breast cancer; however, the role of miR‑93‑5p in retinoblastoma (RB) remains unknown. In the present study, it was reported that miR‑93‑5p expression levels were significantly upregulated in RB tissues compared with in normal tissues by reverse transcription‑quantitative polymerase chain reaction. Furthermore, it was demonstrated via cell counting kit‑8 and Transwell assays that knockdown of miR‑93‑5p significantly suppressed the proliferation, migration and invasion of RB cells, but promoted cellular apoptosis. Regarding the underlying mechanism, the present study reported that phosphatase and tensin homolog (PTEN) was a direct target of miR‑93‑5p in RB cells. Overexpression of miR‑93‑5p significantly inhibited the expression of PTEN; opposing results were observed when PTEN expression was downregulated. Furthermore, the present study revealed that PTEN expression levels were downregulated and were inversely correlated with that of miR‑93‑5p in RB tissues. Additionally, the present study demonstrated that knockdown of PTEN in miR‑93‑5p‑depleted RB cells significantly reversed the effects of miR‑93‑5p on cell proliferation, migration and invasion; miR‑93‑5p knockdown was suggested to promote PTEN expression, consequently inhibiting the activation of phosphoinositide 3‑kinase (PI3K)/protein kinase B (AKT) signaling pathway. Collectively, the results of the present study demonstrated that miR‑93‑5p may serve a role as an oncogene by modulating the PTEN/PI3K/AKT signaling pathway in RB, indicating that miR‑93‑5p may be a potential therapeutic target for the treatment of RB.