<b>The Role of Prolactin in Breast Cancer Metastasis: A Preclinical Study</b>

Background: Prolactin–prolactin receptor signaling has been implicated in breast cancer cell survival, growth, and invasive behavior, although its effects vary according to cellular and molecular context. Objective: To evaluate the effects of prolactin exposure and concurrent prolactin-receptor inhibition on metabolic activity, scratch closure, Matrigel invasion, and selected molecular markers in MCF-7 breast cancer cells. Methods: In this in vitro experimental study, MCF-7 cells were assigned to untreated control, prolactin 50 ng/mL, prolactin 100 ng/mL, and prolactin 100 ng/mL plus prolactin-receptor inhibitor groups. Metabolic activity was assessed using the MTT assay at 24, 48, and 72 hours, while monolayer closure was measured using a scratch assay at 24 and 48 hours. Matrigel invasion and messenger RNA expression of STAT5, MMP-9, BCL-2, and PRLR were also evaluated. Data were summarized as mean ± standard deviation. Results: At 72 hours, MTT absorbance was 0.60 ± 0.04 in controls, 0.79 ± 0.05 with prolactin 50 ng/mL, 1.01 ± 0.06 with prolactin 100 ng/mL, and 0.62 ± 0.04 with prolactin plus inhibitor. At 48 hours, scratch closure was 45.0% ± 3.0%, 62.0% ± 3.4%, 78.0% ± 4.1%, and 48.0% ± 2.8%, respectively. Prolactin-treated cells were reported to demonstrate greater Matrigel invasion and increased expression of STAT5, MMP-9, BCL-2, and PRLR, while receptor inhibition attenuated these responses. Conclusion: Prolactin exposure was associated with increased metabolic activity and scratch closure in MCF-7 cells, whereas PRLR inhibition reduced these effects. Further quantitative and mechanistic validation is required before clinical or therapeutic implications can be established