Abstract
Acute myeloid leukaemia (AML) is a frequently diagnosed malignancy in adults. Long non-coding RNA (lncRNA) colon cancer-associated transcript 1 (CCAT1) has been well known to play vital roles in multiple malignancies including AML. Unfortunately, the detailed mechanism of CCAT1 in AML progression remains obscure. In this study, we demonstrated that CCAT1 was up-regulated in AML samples while its target, miR-490-3p, was relatively down-regulated. CCAT1 markedly increased viability and metastasis of AML cells, while miR-490-3p had opposite effects. CCAT1 could specifically bind to miR-490-3p and reduce its expression and activity, and MAPK1 was a target gene of miR-490-3p. Overexpressed CCAT1 could induce MAPK1 expression and c-Myc reciprocally increased CCAT1 expression. Our data implied that miR-490-3p could be a novel therapeutic target for AML, and highlights the crucial role of CCAT1/miR-490-3p/MAPK1/c-Myc positive feedback loop in AML progression.
A novel long non‑coding RNA TTN‑AS1/microRNA‑589‑5p/FOXP1 positive feedback loop increases the proliferation, migration and invasion of pancreatic cancer cell lines
