RESUMO
It is important to determine the mechanism of liver fibrosis for targeted therapy and the development of targeted therapies for liver fibrosis may offer promise for patients with liver disease. Long noncoding RNAs (lncRNAs) serve a role in hepatic fibrosis. The lncRNA maternally expressed gene 3 (MEG3) has been confirmed to inhibit liver fibrosis. The present study investigated the role of the MEG3 in healthy patients and patients with liver fibrosis. The expression levels of MEG3 and microRNA (miR)145 in the serum of healthy volunteers and patients with liver fibrosis and in LX2 cells were detected using reverse transcriptionquantitative PCR. A dualluciferase reporter assay was used to determine the targeting relationship between MEG3 and miR145, and the targeting relationship between miR145 and peroxisome proliferatoractivated receptor γ (PPARγ). The protein expression levels of PPARγ, αsmooth muscle actin (αSMA) and collagen I (COL1A1) were detected using western blotting. The expression levels of αSMA and COL1A1 were also determined using immunofluorescence. Finally, a Cell Counting Kit8 assay was performed to assess the proliferative ability of LX2 cells. A significantly reduced MEG3 expression level was demonstrated in serum from patients with liver fibrosis compared with serum from healthy controls. TGFß1 induced a significantly decreased MEG3 expression level in LX2 human hepatic stellate cells in vitro. The TGFß1induced increases in cell proliferation and αSMA and COL1A1 protein expression levels were reversed following MEG3 overexpression. The results also demonstrated that MEG3 sponged miR145 and competed endogenously with miR145 to regulate PPARγ. In summary, the present study identified MEG3 as an antifibrotic lncRNA and provided new information regarding the role of MEG3 in liver fibrosis. MEG3 may therefore be a potential target in the treatment of liver fibrosis.