Eomesodermin in renal cell carcinoma: Epigenetic and immune crosstalk driving tumor progression (Review)
- 1Key Laboratory of Reproductive Health Diseases Research and Translation of Ministry of Education, Department of Urology, The First Affiliated Hospital, Hainan Medical University, Haikou, Hainan 570102, P.R. China
- 2Department of Urology, The Second Affiliated Hospital of Hainan Medical University, Haikou, Hainan 570100, P.R. China
Abstract
Renal cell carcinoma (RCC) is the main pathological type of kidney cancer, which accounts for approximately 85-95% of all cases of kidney cancer. Despite the emergence of targeted therapies and immunotherapies, however, the development of resistance remains common. Eomesodermin (Eomes) is a member of the T-box transcription factor family that links both developmental biology and immune regulation with tumor-associated programs. In RCC, its function appears to be context-dependent. In tumor-infiltrating leukocytes, Eomes has been shown to support mature natural killer cell and memory CD8+ T-cell function, whereas persistent or dysregulated Eomes is associated with exhausted CD8+ T cells and Eomes-positive type 1 regulatory T-like immunosuppressive cells. In both intrinsic RCC tumor cells and stromal/endothelial compartments, current knowledge remains relatively limited, and what evidence there is has often been derived from indirect RCC pathway research, other tumor types or developmental models. The present review summarizes Eomes-associated mechanisms in RCC through distinguishing among infiltrating leukocytes, tumor cells and stromal/endothelial compartments, and also through separating direct RCC evidence from indirectly derived mechanistic inferences. Epigenetic regulation, PI3K/Akt/mTOR signaling, Wnt/β-catenin signaling, angiogenesis and therapeutic resistance are also discussed according to the strength of the available evidence. Current data support that Eomes stands as an exploratory biomarker and hypothesis-generating therapeutic node, rather than as an established clinical target. Further research should be performed, however, to validate the cell-type-specific functions of Eomes in RCC tissues, single-cell and spatial datasets, in addition to experimental RCC models.
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BibTeX
@article{che2026eomesodermin,
title = {{Eomesodermin in renal cell carcinoma: Epigenetic and immune crosstalk driving tumor progression (Review)}},
author = {Zhifei Che and Dongwen Huang and Jiaming Lin and Xincen Wang and Rongjin Feng and Xianping Che and Yubin Wang},
journal = {International Journal of Oncology},
year = {2026},
month = sep,
doi = {10.3892/ijo.2026.5941},
url = {https://doi.org/10.3892/ijo.2026.5941},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Eomesodermin in renal cell carcinoma: Epigenetic and immune crosstalk driving tumor progression (Review)
AU - Zhifei Che
AU - Dongwen Huang
AU - Jiaming Lin
AU - Xincen Wang
AU - Rongjin Feng
AU - Xianping Che
AU - Yubin Wang
PY - 2026
DA - 2026/09/18
JO - International Journal of Oncology
DO - 10.3892/ijo.2026.5941
UR - https://doi.org/10.3892/ijo.2026.5941
AB - Renal cell carcinoma (RCC) is the main pathological type of kidney cancer, which accounts for approximately 85-95% of all cases of kidney cancer. Despite the emergence of targeted therapies and immunotherapies, however, the development of resistance remains common. Eomesodermin (Eomes) is a member of the T-box transcription factor family that links both developmental biology and immune regulation with tumor-associated programs. In RCC, its function appears to be context-dependent. In tumor-infiltrating leukocytes, Eomes has been shown to support mature natural killer cell and memory CD8+ T-cell function, whereas persistent or dysregulated Eomes is associated with exhausted CD8+ T cells and Eomes-positive type 1 regulatory T-like immunosuppressive cells. In both intrinsic RCC tumor cells and stromal/endothelial compartments, current knowledge remains relatively limited, and what evidence there is has often been derived from indirect RCC pathway research, other tumor types or developmental models. The present review summarizes Eomes-associated mechanisms in RCC through distinguishing among infiltrating leukocytes, tumor cells and stromal/endothelial compartments, and also through separating direct RCC evidence from indirectly derived mechanistic inferences. Epigenetic regulation, PI3K/Akt/mTOR signaling, Wnt/β-catenin signaling, angiogenesis and therapeutic resistance are also discussed according to the strength of the available evidence. Current data support that Eomes stands as an exploratory biomarker and hypothesis-generating therapeutic node, rather than as an established clinical target. Further research should be performed, however, to validate the cell-type-specific functions of Eomes in RCC tissues, single-cell and spatial datasets, in addition to experimental RCC models.
SN - 1019-6439
SN - 1791-2423
ER -