Glycolysis / Gluconeogenesis；Fatty acid degradation；Tyrosine metabolism；Retinol metabolism；Metabolism of xenobiotics by cytochrome P450；Drug metabolism - cytochrome P450；Metabolic pathways；Chemical carcinogenesis

MEG3 over-expression imposes another level of post-transcriptional regulation, whereas MEG3 overexpression increase the expression of the miR-664 target gene, ADH4, through competitive "sponging" miR-664.

Overexpression of Long Non-coding RNA MEG3 Inhibits Proliferation of Hepatocellular Carcinoma Huh7 Cells via Negative Modulation of miRNA-664

Pancreatic cancer；Cell cycle；Wnt signaling pathway；TGF-beta signaling pathway；Hippo signaling pathway；Adherens junction；Hepatitis B；HTLV-I infection；Pathways in cancer；Colorectal cancer；Chronic myeloid leukemia

In vitro experiments revealed that MALAT1 acted as a positive regulator of osteogenic differentiation by repressing miR-204 expression and activity and thereby promoting expression of osteoblast-specific markers, including alkaline phosphatase, mineralized bone matrix formation and osteocalcin. Mechanistically, we identified Smad4 as a direct target of miR-204. Importantly, MALAT1 could directly interact with miR-204 and overexpression of miR-204 efficiently reversed the upregulation of Smad4 induced by MALAT1. Thus, MALAT1 positively regulated the expression of Smad4 through sponging miR-204, and promoted osteogenic differentiation of VICs.

LncRNA MALAT1 sponges miR-204 to promote osteoblast differentiation of human aortic valve interstitial cells through up-regulating Smad4.

Cell cycle； Wnt signaling pathway；TGF-beta signaling pathway；Hippo signaling pathway；Adherens junction；Hepatitis B；HTLV-I infection；Pathways in cancer； Colorectal cancer；Pancreatic cancer；Chronic myeloid leukemia

Mechanistically, we identified Smad4 as a direct target of miR-204. Importantly, MALAT1 could directly interact with miR-204 and overexpression of miR-204 efficiently reversed the upregulation of Smad4 induced by MALAT1.

LncRNA MALAT1 sponges miR-204 to promote osteoblast differentiation of human aortic valve interstitial cells through up-regulating Smad4.