MiR-103a-3p Promotes Tumorigenesis of Breast Cancer by  Targeting ETNK1

Lei Li; Aifeng Qiu; Yuhua Shi

doi:10.18502/ijph.v53i1.14697

Lei Li Department of General Surgery, The Sixth Affiliated Hospital of Nantong University, Yancheng Third People's Hospital, Yan-cheng, 224000, China
Aifeng Qiu Department of General Surgery, The Sixth Affiliated Hospital of Nantong University, Yancheng Third People's Hospital, Yan-cheng, 224000, China
Yuhua Shi Department of General Surgery, The Sixth Affiliated Hospital of Nantong University, Yancheng Third People's Hospital, Yan-cheng, 224000, China

DOI: https://doi.org/10.18502/ijph.v53i1.14697

Keywords: Breast cancer; miR-103a-3p; Proliferation; Apoptosis

Abstract

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.