Breast cancer（bc）是女性人群中患病率和死亡率最高的人类恶性肿瘤，因此，开发新型有效的bc治疗方案是至关重要的。当前研究的主要目的是探讨CEBPB和THBS2在bc中的功能及其潜在的机制。使用RT-qPCR和Western blot进行RNA和蛋白质的测量。分别进行功能和机制检测，以评估bc生物学行为和基因之间的潜在关联。根据生物信息学分析和实验结果，THBS2在bc组织和细胞系中上调，在bc中可以促进细胞迁移，侵袭和EMT。验证了CEBPB可以促进miR-29a-3p转录，从而负向调节THBS2的表达。救援实验的结果显示，CEBPB可以通过THBS2调节bc细胞的恶性行为。此外，确认CEBPB可以抑制B3GALTL的转录，从而影响THBS2蛋白的O-岐糖基化和分泌。确定THBS2与ITGB1之间的相互作用，并发现THBS2可以激活PI3K/AKT信号通路。综上所述，CEBPB通过抑制THBS2的表达和O-岐糖基化抑制bc细胞的迁移，侵袭和EMT。© The Author(s) 2023. Published by Oxford University Press on behalf of Society for the Study of Reproduction. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

Breast cancer (bc) is the second most common type of human malignancies with highest morbidity and mortality in the female population. Therefore, it is essential to develop novel and effective therapies for bc treatment. The main aim of current study is to investigate the functions of CEBPB and THBS2 in bc and the underlying mechanism. RT-qPCR and western blot were performed for the measurement of RNAs and proteins. Function and mechanism assays were respectively conducted for the evaluation of bc biological behaviors and exploration of potential correlation of genes. According to bioinformatics analyses and experimental results, THBS2, up-regulated in bc tissues and cell lines, could facilitate cell migration, invasion and EMT in bc. CEBPB was validated to facilitate miR-29a-3p transcription, thus negatively modulating THBS2 expression. The results of rescue experiments reflected that CEBPB could regulate the malignant behaviors of bc cells via THBS2. Furthermore, CEBPB was ascertained to inhibit the transcription of B3GALTL to affect THBS2 protein O-fucosylation and secretion. The interaction between THBS2 and ITGB1 was confirmed and THBS2 was found to activate the PI3K/AKT signaling pathway. To conclude, CEBPB could restrain bc cell migration, invasion and EMT via inhibition on THBS2 expression and O-fucosylation.© The Author(s) 2023. Published by Oxford University Press on behalf of Society for the Study of Reproduction. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.