MiRNA-142-3P and FUS can be Sponged by Long Noncoding RNA DUBR to Promote Cell Proliferation in Acute Myeloid Leukemia.

Acute myeloid leukemia (AML) represents a frequently occurring adulthood acute leukemia (AL). Great progresses have been achieved in the treatment of AML, but its pathogenic mechanism remains unclear. This study reported the biological functions of lncRNA DUBR in AML pathogenic mechanism. As a result, lncRNA DUBR showed high expression level within AML, resulting in poor prognosis, especially in M4 AML. In vitro studies elucidated that knockdown of DUBR with small interfering RNA (siRNA) resulted in the suppression of survival and colony formation ability, as well as induction of apoptosis, in AML cells. RNA pull-down assay and computational revealed that DUBR could sponge with miRNA-142-3P and interact with FUS protein. MiRNA-142-3P have a negative correlation with DUBR and overexpression of miRNA-142-3P inhibited cell growth in AML. Meanwhile, DUBR promoted the expression of FUS protein, targeting inhibition of FUS significantly promoted cell apoptosis in AML cell lines. In conclusion, these results revealed new mechanism of lncRNA DUBR in AML malignant behavior, and suggested that the manipulation of DUBR expression could serve as a potential strategy in AML therapy.

miR-454 regulates triglyceride synthesis in bovine mammary epithelial cells by targeting PPAR-γ.

Triglycerides account for 99% of milk fat and play a central role in determining dairy product quality. Many factors influence triglyceride synthesis and milk fat secretion. MicroRNAs have been verified to be involved in numerous biological processes, but little is known about their roles in milk fat biosynthesis. In this study, we aim to explore whether miR-454 could regulate triglyceride synthesis in bovine mammary epithelial cells (BMECs) by targeting PPAR-γ. A luciferase reporter assay showed that the predicted target site was correct and that miR-454 and PPAR-γ had a direct interaction. In addition, miR-454 mimics and inhibitors were transfected into BMECs. The results showed that both the mRNA and protein levels of PPAR-γ were negatively correlated with miR-454 expression. Fat droplet accumulation and triglyceride production were also inversely correlated with miR-454 expression. Our results indicate that miR-454 regulates triglyceride synthesis by directly targeting the PPAR-γ 3' UTR in BMECs, suggesting that miR-454 could potentially be a new factor to elevate dairy product quality.