miR-409 expression

This study demonstrated that the miRNA-409-5p/KDM4D/HIF1β/VEGF-A signaling pathway could serve as a novel target for the development of therapeutic strategies for the treatment of imatinib-resistance in GIST patients.

In a xenograft mouse model, miR-409-3p-overexpressed THP-1 cells resulted in much less tumor weight and size in the mice bearing the cells as compared to the mock-transfected mice. Collectively, our findings demonstrated that miR-409-3p exerted tumor suppressor gene effects in AML by directly targeting Rab10, which might provide a promising therapeutic target for AML.

miR-409-3p may prevent non-small cell lung cancer (NSCLC) by affecting ELF2 transcription and other cellular regulators to regulate A549 cell division and induce apoptosis.

Cell proliferation and invasion of miR-409 mimic and SATB1 co-transfected MDA-MB-453 cells increased compared with that of miR-409 mimic-transfected cells, while miR-409 inhibitor and siSATB1 co-transfected BT-549 cells showed the opposite result. All these results indicated that miR-409 regulates breast cancer proliferation and invasion by targeting SATB1 and might be a potential therapeutic target for the treatment of breast cancer.

PDK1 acted as a target gene of miR-409-3p, and PDK1 could be positively and indirectly modulated by circ_0000418 in glioma cells. In summary, circ_0000418 enhances glioma cell growth and accelerates cell cycle progression by regulating miR-409-3p/PDK1 axis.

The down-regulation of miR-409 was conducive to the proliferation, migration and invasion of PC cells. miR-409 is a tumor suppressor of PC, the clinical significance of miR-409 in pancreatic cancer and related tumor cell function was clarified.

In conclusion, MGMT inhibition could suppress the proliferation, invasion, migration and autophagy and promote the apoptosis of PanC-1/GEM cells in vitro and in vivo. PVT1 silencing may affect the PanC-1/GEM cells through changing the MGMT expression by inhibiting the SHH/GLI signaling pathway.