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Integrative Single-Cell and Spatial Transcriptomic Analysis Reveals MAIT Cell Dysfunction in Relapsed HCC.

Geon Woo Park1,2,3, Hayoung Jang1,2, Thuy Nguyen-Phuong4

  • 1Department of Biomedical Sciences, Seoul National University Graduate School, Seoul, Republic of Korea.

Journal of Hepatocellular Carcinoma
|March 25, 2026
PubMed
Summary
This summary is machine-generated.

Relapsed hepatocellular carcinoma (HCC) shows increased malignant hepatocytes and altered mucosal-associated invariant T (MAIT) cells. These MAIT cells in relapsed HCC are dysfunctional and linked to poorer survival.

Keywords:
hepatocellular carcinomamucosal-associated invariant t cellstumor microenvironmenttumor-infiltrating lymphocytes

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Area of Science:

  • Oncology
  • Immunology
  • Genomics

Background:

  • Hepatocellular carcinoma (HCC) recurrence is common after treatment.
  • The tumor immune microenvironment influences HCC progression.
  • The role of mucosal-associated invariant T (MAIT) cells in relapsed HCC is unclear.

Purpose of the Study:

  • To investigate MAIT cell characteristics in relapsed HCC.
  • To analyze MAIT cells' spatial and transcriptional features.
  • To explore associations with malignant hepatocyte phenotypes.

Main Methods:

  • Paired single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics on HCC samples.
  • Analysis of 49,229 cells with quality control and batch correction.
  • Identification of malignant hepatocytes and MAIT cell states.

Main Results:

  • Relapsed HCC exhibits increased malignant hepatocytes with stemness signatures.
  • MAIT cells are significantly enriched in relapsed tumors.
  • Relapsed MAIT cells show a dysfunctional phenotype and interact more with malignant hepatocytes.
  • High MAIT cell signature scores correlate with poorer overall survival in HCC patients.

Conclusions:

  • Relapsed HCC is characterized by enhanced malignant hepatocyte stemness.
  • Altered MAIT cell states, including dysfunction, are observed in the relapsed tumor microenvironment.
  • MAIT cell dysregulation may be linked to relapse-specific HCC biology, requiring further study.