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Targeting B7-H1 (PD-L1) Sensitizes Cancer Cells to Chemotherapy

Targeting B7-H1 (PD-L1) Sensitizes Cancer Cells to Chemotherapy

Xiaosheng Wu, Yanli Li, Xin Liu, Chunhua Chen, Susan M Harrington, Siyu Cao, Tiancheng Xie, Tu Pham, Aaron S Mansfield, Yiyi Yan, Eugene D Kwon, Liewei Wang, Kun Ling, Haidong Dong

Heliyon. 2018 Dec 18;4(12):e01039.

PMID: 30603685

Abstract:

Development of resistance to chemotherapy is a major obstacle in extending the survival of patients with cancer. Although originally defined as an immune checkpoint molecule, B7-H1 (also named as PD-L1 or CD274) was found to play a role in cancer chemoresistance; however, the underlying mechanism of action of B7-H1 in regulation of chemotherapy sensitivity remains unclear in cancer cells. Here we show that development of chemoresistance depends on an increased activation of ERK in cancer cells overexpressing B7-H1. Conversely, B7-H1 knockout (KO) by CRISPR/Cas9 renders human cancer cells susceptible to chemotherapy in a cell-context dependent manner through a reduced activation of p38 MAPK. B7-H1 was found to associate with the catalytic subunit of DNA-dependent protein kinase (DNA-PKcs) and this association promoted or maintained the activation of ERK or p38 MAPK in cancer cells. Importantly, we found that targeting B7-H1 by anti-B7-H1 monoclonal antibody (H1A) increased the sensitivity of human triple negative breast cancer cells to cisplatin therapy in vivo. Our results suggest that targeting B7-H1 by an antibody capable of disrupting B7-H1 signals may be a new approach to sensitize cancer cells to chemotherapy.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR42413193	PD-L1/CD274/B7-H1 human			Price

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