Long Noncoding RNA MALAT1 Acts as a Competing Endogenous RNA to Regulate TGF-β2 Induced Epithelial-Mesenchymal Transition of Lens Epithelial Cells by a MicroRNA-26a-Dependent Mechanism
Figure 1
TGF-β2 induces different expression of lncRNAs in primary HLECs. (a) Heat map showed the mostly significant differential expression of lncRNAs in Primary HLECs by human lncRNA Array v2.0. The primary HLECs were treated with TGF-β2 (5 ng/ml) for 48 h which were experiment groups. The primary HLECs were treated without TGF-β2 which were control groups. (b) The expression of XIST, CCAT1, NEAT1, and MALAT1 was tested in human PCO attached LECs (n=16) and normal attached LECs (n=15) by qRT-PCR. P < 0.05 compared with PCO attached LECs. (c) The expression of XIST, CCAT1, NEAT1, and MALAT1 was detected in LECs obtained from patients with anterior polar cataracts (n=33) and patients with nuclear cataracts (n=33) using qRT-PCR. P < 0.05 compared with anterior polar cataracts. (d) qRT-PCR showed that the indicated concentration of TGF-β2 induces over-expression of MALAT1 in primary HLECs in a dose-dependent manner. P < 0.05 compared with group without TGF-β2. (e) qRT-PCR showed that the indicated time of 5 ng/ml TGF-β2 induces overexpression of MALAT1 in primary HLECs in a time-dependent manner. P < 0.05 compared with group without TGF-β2. (b, c, d, and e) The data are presented as the mean± SE of six independent experiments.