Neonicotinoids are insecticides used worldwide for fruits and vegetables. Imidacloprid (IMI) is among the 10 most detected agrochemicals in studies in Argentina and Brazil, with a prolonged residual effect in the soil, accumulating due to its repeated application, and may affect human health. IMI increases the expression of aromatase and the secretion of estradiol in breast cancer cells, so exposure to IMI could collaborate with tumor development and progression, stimulating estrogen receptor (ER) pathways such as G protein-associated ER (GPER). Some endocrine disruptors activate the aryl hydrocarbon receptor (AhR), a transcription factor that modulates processes such as inflammation, proliferation and migration. The indoleamine 2,3-dioxygenase (IDO) produces kynurenine, which is involved in modulating the immunosuppressive microenvironment in tumors. Our objective was to examine whether exposure of HER2(+) LM3 breast cancer cells to IMI (0.01, 0.1, 1 and 10 μM) alters cell viability, proliferation and migration, as well as the activity of metalloprotease (MMP)9, and whether these effects are mediated by the AhR, IDO and GPER pathways using specific inhibitors. In addition, we studied its action on the expression protein of AhR, GPER and its downstream pathway ERK1/2. Our results showed that IMI (10 μM) increases cell viability at 48 h (p<0.05) (MTT assay) and proliferation (clonogenic assay) (p<0.05) through AhR and GPER pathways in LM3 cells. Low doses of IMI (0.01 and 0.1 μM) enhance cell migration (wound healing assay) (p<0.01) in a manner dependent on AhR, GPER and IDO. The activity of MMP-9 (gel zymography) shows a tendency to increase with IMI (1-10 μM). Furthermore, exposure to IMI enhances GPER and ERK1/2 expression by WB at 0.1 μM (p<0.05), showing a tendency to reduce AhR levels at 0.01 and 0.1 μM. All these findings suggest that exposure of populations to IMI could contribute to the development and progression of HER2-positive breast cancer.