biostudies-literatureUnknown10(1)Cheng LEvidence suggests that metformin might be a potential candidate for breast cancer treatment. Yet, its relevant molecular mechanisms remain to be fully investigated. We found that metformin could suppress the N6-methyladenosine (m⁶A) level in breast cancer cells significantly. The latter has an essential role in breast cancer progression and is newly considered as a therapeutic target. In this study, we measured the m⁶A level by m⁶A colorimetric analysis and dot blot assay. We then performed qRT-PCR, western blot, MeRIP, dual-luciferase reporter assay, and others to explore the m⁶A-dependent pathway associated with metformin. In vivo effect of metformin was investigated using a mouse tumorigenicity model. In addition, breast cancer and normal tissOncogenesis7https://www.ebi.ac.uk/biostudies/studies/S-EPMC7801402biostudies-literatureMetformin exhibits antiproliferation activity in breast cancer via miR-483-3p/METTL3/m⁶A/p21 pathway.PMC7801402Shi LLi ZZhou XJWei JFHuang YZDai XYZhang XCheng LDing QXu LYZhu YLfalseMetformin exhibits antiproliferation activity in breast cancer via miR-483-3p/METTL3/m⁶A/p21 pathway.Evidence suggests that metformin might be a potential candidate for breast cancer treatment. Yet, its relevant molecular mechanisms remain to be fully investigated. We found that metformin could suppress the N6-methyladenosine (m⁶A) level in breast cancer cells significantly. The latter has an essential role in breast cancer progression and is newly considered as a therapeutic target. In this study, we measured the m⁶A level by m⁶A colorimetric analysis and dot blot assay. We then performed qRT-PCR, western blot, MeRIP, dual-luciferase reporter assay, and others to explore the m⁶A-dependent pathway associated with metformin. In vivo effect of metformin was investigated using a mouse tumorigenicity model. In addition, breast cancer and normal tiss2021-01-01T00:00:00Z2021 Jan2025-05-31T23:35:04.186Z2025-05-31T23:35:04.186ZS-EPMC78014023343179010.1038/s41389-020-00290-y