miR-155 Directly Targets MARCH7 and Modulates Viability and Invasive Phenotypes in Breast Cancer Cells.

miR-155 is an oncogenic microRNA implicated in breast cancer, but its downstream post-transcriptional targets remain incompletely defined. This study tested membrane-associated RING-CH 7 (MARCH7) as a direct miR-155 target and examined associated molecular and cellular phenotypes in MCF-7 and MDA-MB-231 breast cancer cells. Basal miR-155 expression was assessed in MCF-10A, MCF-7, and MDA-MB-231 cells. MCF-7 cells were analyzed by MTT, RT-qPCR, Western blotting, bioinformatic prediction, dual-luciferase reporter assays, and MARCH7 knockdown; MDA-MB-231 cells were additionally evaluated by MTT, RT-qPCR, wound-healing, and Transwell invasion assays. miR-155 was more abundant in the breast cancer cell lines than in MCF-10A cells. In MCF-7 cells, miR-155 overexpression increased MTT-derived metabolic viability, reduced MARCH7 and PTEN expression, increased Cyclin D1, reduced cleaved caspase-3, and was associated with increased PI3K and AKT phosphorylation. In MDA-MB-231 cells, RT-qPCR confirmed successful miR-155 modulation, whereas MTT changes were modest; these small changes may reflect either model/endpoint differences or limited sensitivity of the MTT assay under the tested conditions. Dual-luciferase assays confirmed direct targeting of the MARCH7 3'-UTR by miR-155, while miR-155 inhibition markedly reduced MDA-MB-231 migration and invasion. These findings establish MARCH7 as a direct miR-155 target in the models examined. The PTEN/PI3K/AKT changes are associated downstream findings and are not yet proven to be mediated specifically by MARCH7.