TEM8 marks neovasculogenic tumor-initiating cells in triple-negative breast cancer

Jiahui Xu, Xiaoli Yang, Qiaodan Deng, Cong Yang, Dong Wang, Guojuan Jiang, Xiaohong Yao, Xueyan He, Jiajun Ding, Jiankun Qiang, Juchuanli Tu, Rui Zhang, Qun-Ying Lei, Zhi-min Shao, Xiuwu Bian (), Ronggui Hu (), Lixing Zhang () and Suling Liu ()
Additional contact information
Jiahui Xu: Fudan University
Xiaoli Yang: Fudan University
Qiaodan Deng: Fudan University
Cong Yang: School of Medicine, Guizhou University
Dong Wang: WPI Nano Life Science Institute, Kanazawa University, Kakuma-machi
Guojuan Jiang: Fudan University
Xiaohong Yao: Institute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University); Key Laboratory of Tumor Immunopathology, Ministry of Education of China
Xueyan He: Fudan University
Jiajun Ding: Fudan University
Jiankun Qiang: Fudan University
Juchuanli Tu: Fudan University
Rui Zhang: Fudan University
Qun-Ying Lei: Fudan University
Zhi-min Shao: Fudan University
Xiuwu Bian: Institute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University (Army Medical University); Key Laboratory of Tumor Immunopathology, Ministry of Education of China
Ronggui Hu: Chinese Academy of Sciences
Lixing Zhang: Fudan University
Suling Liu: Fudan University

Nature Communications, 2021, vol. 12, issue 1, 1-15

Abstract: Abstract Enhanced neovasculogenesis, especially vasculogenic mimicry (VM), contributes to the development of triple-negative breast cancer (TNBC). Breast tumor-initiating cells (BTICs) are involved in forming VM; however, the specific VM-forming BTIC population and the regulatory mechanisms remain undefined. We find that tumor endothelial marker 8 (TEM8) is abundantly expressed in TNBC and serves as a marker for VM-forming BTICs. Mechanistically, TEM8 increases active RhoC level and induces ROCK1-mediated phosphorylation of SMAD5, in a cascade essential for promoting stemness and VM capacity of breast cancer cells. ASB10, an estrogen receptor ERα trans-activated E3 ligase, ubiquitylates TEM8 for degradation, and its deficiency in TNBC resulted in a high homeostatic level of TEM8. In this work, we identify TEM8 as a functional marker for VM-forming BTICs in TNBC, providing a target for the development of effective therapies against TNBC targeting both BTIC self-renewal and neovasculogenesis simultaneously.

Date: 2021
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DOI: 10.1038/s41467-021-24703-7

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