VMP1 inhibits the progression of breast cancer via regulating PI3K/AKT and MEK/ERK signaling pathway.

[BACKGROUND] Vacuolar membrane protein 1 (VMP1) is an endoplasmic reticulum - resident and multi - spanning membrane protein involved in various human cancers. However, its biological functions and molecular mechanisms in breast cancer remain underexplored.

[METHODS] Gene expression profiling was used to determine VMP1 levels. Western blot, qRT - PCR, and single - cell analysis were employed to confirm the findings. Functional assays such as knockdown and overexpression experiments were carried out to assess the effects on cell proliferation, colony formation, and migration. In vivo tumor growth experiments were also conducted. Additionally, clinical analysis of 117 breast cancer patient samples was performed to study the correlation between VMP1 expression and molecular subtypes.

[RESULTS] VMP1 was significantly upregulated in MCF − 7 cells line. Knockdown of VMP1 enhanced cell proliferation, colony formation, and migration, while overexpression suppressed tumor cell malignancy and inhibited tumor growth in vivo. Mechanistically, VMP1 was found to regulate key oncogenic signaling pathways, including PI3K/AKT and MEK/ERK. Clinical analysis showed that VMP1 expression was correlated with molecular subtypes.

[CONCLUSIONS] In conclusion, our findings suggest that VMP1 plays a crucial role in breast cancer progression, and modulation of its expression or activity may offer a therapeutic strategy.

[SUPPLEMENTARY INFORMATION] The online version contains supplementary material available at 10.1186/s12935-025-04149-3.