생화학분자생물학회

	Name: Jeong-Seok Nam ( namje@gist.ac.kr )
	2016 – Present	Associate Professor, Professor, Department of Life Sciences (formerly School of Life Sciences), Gwangju Institute of Science and Technology, Korea
	2007 – 2016	Assistant Professor, Associate Professor, Department of Molecular Medicine, School of Medicine, Gachon University of Medicine and Science (now Gachon University), Korea
	2003 – 2007	Postdoctoral Fellow, Laboratory of Cell Regulation and Carcinogenesis, National Cancer Institute, USA
	1999 – 2002	Postdoctoral Research Associate, Pathology Division, National Cancer Center Research Institute, Japan
	1994 – 1999	MS / PhD, College of Veterinary Medicine, Seoul National University, Korea

The multifaceted role of YAP in the tumor microenvironment and its therapeutic implications in cancer

The tumor microenvironment (TME) plays a critical role in cancer progression, immune evasion and therapeutic resistance. The transcriptional coactivators YAP and TAZ, key effectors of the Hippo signaling pathway, have emerged as central regulators of TME remodeling. YAP/TAZ are activated in both tumor and stromal compartments, where they function as mechanotransducers and integrate canonical Hippo pathway suppression, noncanonical microenvironmental cues and genetic or epigenetic signals to drive transcriptional programs. These changes collectively facilitate tumor immune evasion. YAP/TAZ further promote angiogenesis and upregulate PD-L1 expression in tumor cells and cancer-associated fibroblasts, and a subset of immunosuppressive cells in the TME, contributing to resistance to ICB. In addition to their tumor-intrinsic and stromal functions, YAP/TAZ impair antitumor immunity by altering immune cell differentiation and dampening effector responses. Targeting the YAP/TAZ-TEAD axis has shown potential efficacy when combined with immune checkpoint inhibitors, chimeric antigen receptor T cell therapies and tumor vaccines. Although challenges such as tumor selectivity and resistance mechanisms persist, advances in single-cell and spatial transcriptomics are enabling the dissection of YAP/TAZ-regulated networks and guiding the development of more precise therapeutic strategies. Collectively, YAP/TAZ inhibition offers a promising avenue to reprogram the TME and enhance the efficacy of next-generation cancer immunotherapies.


Exp Mol Med. 2025 Oct;57(10):2201-2213. doi: 10.1038/s12276-025-01551-9.
https://pubmed.ncbi.nlm.nih.gov/41028521/