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Glioma is one of the most common types of malignant cancer and the significance of microRNAs (miRNAs) in cancer therapy has been demonstrated. In the current study, miR-490-3p expression was significantly downregulated in glioma tissue and cell lines. Overexpression of miR-490-3p inhibited glioma cell proliferation and migration in vitro. In addition, the high-mobility group AT-hook 2 (HMGA2) was identified as a candidate target gene of miR-490-3p. The current study demonstrated that miR-490-3p mimic could inhibit HMGA2 protein expression in glioma cells. In addition, correlation analysis demonstrated that miR-490-3p and HMGA2 expression was inversely correlated in glioma tissues. Furthermore, the inhibitory effect of miR-490-3p mimic on cell proliferation and migration was partially reversed by the overexpression of HMGA2. Taken together, these results suggest that miR-490-3p may have a tumor suppressive role in glioma and therefore miR-490-3p may be a new target for the treatment of glioma. [ABSTRACT FROM AUTHOR]

Triple negative breast cancer (TNBC) has received increasing attention from oncologists worldwide due to its poor prognosis and paucity of targeted therapies. MicroRNAs (miRs) are a group of small non‑coding RNAs that are responsible for the post‑transcriptional regulation of various target genes. The present study demonstrated that the expression of miR‑199b‑5p in breast cancer tissue was significantly reduced compared with that in normal breast tissues by reverse transcription‑quantitative polymerase chain reaction. In addition, western blot analysis and luciferase reporter assays revealed that miR‑199b‑5p in TNBC cells inhibited discoidin domain receptor tyrosine kinase 1 expression by directly targeting its 3'‑untranslated region. Furthermore, miR‑199b‑5p markedly suppressed the proliferation and invasion of TNBC cells, as demonstrated by using wound‑healing, migration, invasion and proliferation assays. Collectively, these results indicate that miR‑199b‑5p may be a novel alternative therapeutic target for TNBC. [ABSTRACT FROM AUTHOR]