Li Lei, Qiu Aifeng, Shi Yuhua
Department of General Surgery, The Sixth Affiliated Hospital of Nantong University, Yancheng Third People's Hospital, Yancheng, 224000, China.
Iran J Public Health. 2024 Jan;53(1):208-218. doi: 10.18502/ijph.v53i1.14697.
We aimed to elucidate the molecular mechanism of miR-103a-3p regulating breast cancer progression.
Firstly, clinical tissues was obtained from 2019-2023 at Yancheng Third People's Hospital, Yancheng, China. miR-103a-3p or expression in clinical tissues or breast cancer cell lines was analyzed with qRTPCR. 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.
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, 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.
miR-103a-3p might promote breast cancer progression by inhibiting .
我们旨在阐明miR-103a-3p调控乳腺癌进展的分子机制。
首先,于2019年至2023年在中国盐城第三人民医院获取临床组织。采用qRT-PCR分析临床组织或乳腺癌细胞系中miR-103a-3p的表达情况。对MDA-MB-231细胞进行miR-103a-3p抑制剂或模拟物处理,并过表达ETNK1。通过CCK-8和TUNEL检测法检测细胞增殖和凋亡能力。将转染后的MDA-MB-231细胞接种到BALB/c小鼠体内建立异种移植模型。
miR-103a-3p在乳腺癌中呈过表达,且与预后不良相关。缺失miR-103a-3p的MDA-MB-231细胞显示出较弱的细胞增殖水平和较高的凋亡率。相反,(此处原文缺失具体基因名)在乳腺癌中表达下调,并被证明是miR-103a-3p的下游靶点。接受miR-103a-3p拮抗剂治疗或ETNK1基因敲低的异种移植模型均导致肿瘤生长受到抑制。
miR-103a-3p可能通过抑制(此处原文缺失具体基因名)促进乳腺癌进展。