Tehran University of Medical Sciences Iranian Journal of Public Health 2251-6085 53 1 2024 01 01 208 218 Yuhua Shi Department of General Surgery, The Sixth Affiliated Hospital of Nantong University, Yancheng Third People's Hospital, Yancheng, 224000, China Lei Li Department of General Surgery, The Sixth Affiliated Hospital of Nantong University, Yancheng Third People's Hospital, Yancheng, 224000, China Aifeng Qiu Department of General Surgery, The Sixth Affiliated Hospital of Nantong University, Yancheng Third People's Hospital, Yancheng, 224000, China 2023 05 18 2023 08 12 Background: We aimed to elucidate the molecular mechanism of miR-103a-3p regulating breast cancer progression. Methods: Firstly, clinical tissues was obtained from 2019-2023 at Yancheng Third People's Hospital, Yancheng, China. miR-103a-3p or ETNK1 expression in clinical tissues or breast cancer cell lines was analyzed with qRT-PCR. MDA-MB-231 cells were performed with miR-103a-3p inhibitor or mimic, and OE-ETNK1. The proliferation and apoptosis ability were detected by CCK-8 and TUNEL assay. The xenograft models were established by inoculating transfected MDA-MB-231 cells to BALB/c mice. Results: miR-103a-3p showed an overexpression and was related to poor prognosis in breast cancer. miR-103a-3p-deprived MDA-MB-231 cells displayed weaker levels of cell proliferation and higher rates of apoptosis. In contrast, ETNK1 was downregulated in breast cancer and proved to be a downstream target of miR-103a-3p. Xenograft models subjected to either miR-103a-3p antagomir treatment or ETNK1-knockdown resulted in tumor growth suppression. Conclusion: miR-103a-3p might promote breast cancer progression by inhibiting ETNK1.Breast cancer https://ijph.tums.ac.ir/index.php/ijph/article/view/32066 https://ijph.tums.ac.ir/index.php/ijph/article/download/32066/8145