MicroRNA‑363‑3p inhibits cell proliferation and induces apoptosis in retinoblastoma cells via the Akt/mTOR signaling pathway by targeting PIK3CA
- Xiaojie Ma
- Lan Jin
- Xiaoqin Lei
- Jingan Tong
- Runsheng Wang
Affiliations: Department of Ophthalmology, Xi'an Hospital of Traditional Chinese Medicine, Xi'an, Shaanxi 710021, P.R. China, Department of Ophthalmology, Xi'an No. 4 Hospital, Xi'an, Shaanxi 710004, P.R. China, Department of Ophthalmology, The First Affiliated Hospital of Shaanxi University of Chinese Medicine, Xianyang, Shaanxi 712000, P.R. China
- Published online on: March 12, 2020 https://doi.org/10.3892/or.2020.7544
Copyright: © Ma
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
There is extensive evidence suggesting that microRNAs (miRs) can modulate the activity of oncogenes and tumor suppressors, and are associated with the occurrence of cancer. In the present study, the function of miR‑363‑3p in the progression of retinoblastoma (RB) was investigated. miR‑363‑3p expression in RB was decreased, and miR‑363‑3p protein levels were found to be inversely correlated with phosphatidylinositol‑4,5‑bisphosphate 3‑kinase catalytic subunit α (PIK3CA) levels. Overexpression of miR‑363‑3p in an in vitro model of RB revealed that miR‑363‑3p had anticancer effects on RB and regulated PIK3CA, pyruvate dehydrogenase kinase 1 (PDK1) and phosphorylated protein kinase B (p‑AKT) protein expression. Downregulation of miR‑363‑3p promoted cell proliferation of RB cells through PIK3CA, PDK1 and p‑AKT protein expression. Knockdown of PIK3CA increased the anticancer effects of miR‑363‑3p in RB cells. Treatment with OSU‑03012, a PDK1 inhibitor, accelerated the anticancer effects of miR‑363‑3p in RB cells. Taken together, the results demonstrate that miR‑363‑3p functions as a tumor suppressor in RB by targeting PIK3CA.