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image of Association of KIM-1 (HAVCR1) Expression with the Tumor Immune Microenvironment in Clear Cell Renal Cell Carcinoma

Abstract

Introduction

Kidney injury molecule 1 (KIM-1) is a cell-surface glycoprotein expressed in the proximal tubules and encoded by the hepatitis A virus cellular receptor 1 () gene. It is also expressed in renal cell carcinoma (RCC).

Objective

This study examined the immune landscape of clear cell RCC in association with expression.

Methods

Next-generation sequencing (NGS) data from ccRCC tumor samples of patients from The Cancer Genome Atlas (TCGA) were interrogated for enrichment of immune infiltrates and checkpoints in tumors harboring high mRNA expression or/and amplification.

Results

mRNA expression was positively associated with presence of CD8+ (r = 0.254, = 3.03 x 10-8) and CD4 T-cells (r = 0.329, = 3.98 x 10-13), while it was negatively associated with T-regulatory (T-regs) (r = ̶ 0.2, = 1.47 x 10-5) and myeloid-derived suppressor cells (MDSCs) (r = ̶.0.285, = 4.92 x 10-10). amplification was also associated with CD8+ ( = 0.0019), CD4+ T cells ( = 0.0002) while expression of gene was positively associated with immune checkpoints PD-L1 () (r = 0.331, = 4.64 x 10-15) and mRNA expression (r = 0.085, = 0.05). transcript levels were directly correlated with those of Polybromo-1 () (r = 0.276, = 9.36 x 10-11) while inversely related with BRCA-associated protein 1 () gene expression (r = ̶ 0.134, = 1.94 x 10-3).

Discussion

The study reveals that high (KIM-1) expression in clear cell RCC is associated with a distinct immune profile characterized by increased CD8+/CD4+ T-cell infiltration and immune checkpoint expression, suggesting a potential role in predicting immunotherapy response, though the observational nature and reliance on TCGA data limit causal inference.

Conclusions

Collectively, a potential immune-regulatory role of KIM-1 in clear cell RCC is implicated. This could be exploited for predicting benefit from adjuvant immunotherapy.

This is an open access article published under CC BY 4.0 https://creativecommons.org/licenses/by/4.0/legalcode
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2025-07-28
2025-10-29
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