癌症研究
转移
Wnt信号通路
基因敲除
乳腺癌
免疫疗法
免疫检查点
上皮-间质转换
癌症
生物
医学
免疫系统
免疫学
细胞凋亡
信号转导
内科学
细胞生物学
生物化学
作者
Xing Chang,Jingang Liu,Qian Yang,Yu Gao,Xiaoxue Li,Junjun Zhao,Yang Li,Zi Liu,Zengqiang Li,Yingliang Wu,Daiying Zuo
标识
DOI:10.1016/j.bcp.2023.115582
摘要
Metastasis is an obstacle to the clinical treatment of aggressive breast cancer (BC). Studies have shown that high mobility group A1 (HMGA1) is abnormally expressed in various cancers and mediates tumor proliferation and metastasis. Here, we provided more evidence that HMGA1 mediated epithelial to mesenchymal transition (EMT) through the Wnt/β-catenin pathway in aggressive BC. More importantly, HMGA1 knockdown enhanced antitumor immunity and improved the response to immune checkpoint blockade (ICB) therapy by upregulating programmed cell death ligand 1 (PD-L1) expression. Simultaneously, we revealed a novel mechanism by which HMGA1 and PD-L1 were regulated by the PD-L1/HMGA1/Wnt/β-catenin negative feedback loop in aggressive BC. Taken together, we believe that HMGA1 can serve as a target for the dual role of anti-metastasis and enhancing immunotherapeutic responses.
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