2. Academic Validation
  3. Targeting HMGA1 contributes to immunotherapy in aggressive breast cancer while suppressing EMT

Targeting HMGA1 contributes to immunotherapy in aggressive breast cancer while suppressing EMT

  • Biochem Pharmacol. 2023 May 3;115582. doi: 10.1016/j.bcp.2023.115582.
Xing Chang 1,  Jingang Liu 1,  Qian Yang 1,  Yu Gao 2,  Xiaofei Ding 3,  Junjun Zhao 2,  Yang Li 1,  Zi Liu 1,  Zengqiang Li 1,  Yingliang Wu 1,  Daiying Zuo 4
Affiliations

Affiliations

  • 1 Department of Pharmacology, Shenyang Pharmaceutical University, 103 Wenhua Road, Shenhe District, Shenyang 110016, China.
  • 2 Dalian Municipal Central Hospital Affiliated of Dalian Medical University, Dalian, 116033, China.
  • 3 Department of pharmacology, School of Medicine, Taizhou University, 1139 Shi-Fu Avenue, Taizhou 318000, China.
  • 4 Department of Pharmacology, Shenyang Pharmaceutical University, 103 Wenhua Road, Shenhe District, Shenyang 110016, China. Electronic address: zuodaiying@syphu.edu.cn.
PMID: 37146833 DOI: 10.1016/j.bcp.2023.115582
Abstract

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.

Keywords

HMGA1; PD-L1; aggressive breast cancer; antitumor immunity; metastases.

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