MiR‑200c‑3p regulates the proliferation and apoptosis of human trabecular meshwork cells by targeting PTEN.

Abstract

Glaucoma is an optic neuropathy that may lead to visual field loss and blindness. Human trabecular meshwork (HTM) cell dysfunction increases intraocular pressure, which leads to glaucoma. microRNAs (miRs) are single‑stranded non‑coding RNAs that regulate cellular processes in HTM cells. The aim of the present study was to evaluate the role of miR‑200c‑3p in HTM cells. HTM cells were treated with 300µM H2O2, and the expression of miR‑200c‑3p was measured by reverse transcription‑quantitative polymerase chain reaction. The expression of miR‑200c‑3p was significantly downregulated under oxidative stress. Phosphatase and tensin homolog (PTEN) was predicted to be a potential target of miR‑200c‑3p using TargetScan, and this was confirmed by a dual‑luciferase reporter assay. The expression of PTEN was upregulated in H2O2‑treated HTM cells. In addition, PTEN expression was negatively regulated by miR‑200c‑3p. Then, cell proliferation and apoptosis were measured by Cell Counting Kit‑8 and flow cytometry assays, respectively. The results demonstrated that the overexpression of miR‑200c‑3p enhanced cell proliferation and inhibited cell apoptosis, while PTEN reversed the effects of miR‑200c‑3p. In addition, miR‑200c‑3p suppressed the expression of PTEN, cleaved caspase‑3 and Bax, and improved the expression of phosphorylated (p)‑AKT, AKT and p‑serine/threonine‑protein kinase mTOR (mTOR), while PTEN attenuated these effects. Taken together, these data suggested that overexpression of miR‑200c‑3p targets PTEN to suppress cleaved caspase‑3 and Bax expression and activate the PTEN/AKT/mTOR signaling pathway, thereby resulting in the promotion of cell proliferation and the inhibition of cell apoptosis. These results revealed the role of miR‑200c‑3p in HTM cells and its underlying molecular mechanism, which may provide a potential target for the treatment of patients with glaucoma.