Purpose: To investigate the role and mechanism of formin-like protein 1 (FMNL1) in breast cancer progression. Methods: Expression of FMNL1 in breast cancer cells was evaluated using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and western blotting. Colony formation and CCK8 assays were performed to assess cell proliferation. Cell migration and invasion were determined using wound-healing and Transwell assays, respectively. Results: Data from UALCAN prediction (http://ualcan.path.uab.edu/analysis.html) showed that FMNL1 was significantly upregulated in primary breast cancer tissue compared to normal tissue (p < 0.01). Enhanced FMNL1 mRNA and protein expression was also identified in breast cancer cells. shRNAmediated FMNL1 knockdown decreased viability of breast cancer cells and reduced cell proliferation, migration, and invasion. Expression of protein high mobility group AT-hook 1 (HMGA1) was reduced, whereas breast cancer gene 1 (BRCA1) expression was enhanced, in breast cancer cells transfected with shRNA-FMNL1. Overexpression of HMGA1 attenuated FMNL1-knockdown-induced decreased HMGA1 expression and increased BRCA1 expression in breast cancer cells. BRCA1 knockdown counteracted the suppressive effects of FMNL1 silencing on breast cancer cell proliferation, migration, and invasion. Conclusion: FMNL1 promotes breast cancer cell growth and metastasis by inhibiting BRCA1 via upregulation of HMGA1, providing a potential therapeutic target for breast cancer.