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Published on: August 7, 2020

Tumor microenvironment and metabolic reprogramming in MASLD-related hepatocellular carcinoma

Vanilla X Zhang1, Tiffany C-Y Yu2, Yu M Tsui2

  • 1Department of Pathology, School of Clinical Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong; State Key Laboratory of Liver Research, The University of Hong Kong, Hong Kong; Department of Pathology, The University of Hong Kong-Shenzhen Hospital, Shenzhen, China.

Trends in Molecular Medicine
|May 14, 2026
PubMed

Insights

Metabolic dysfunction-associated steatotic liver disease (MASLD) fuels liver cancer. Understanding the tumor microenvironment

Area of Science:

  • Hepatology and Oncology
  • Metabolic Diseases
  • Cancer Biology

Background:

  • Metabolic dysfunction-associated steatotic liver disease (MASLD) is a major driver of hepatocellular carcinoma (HCC).
  • The intricate mechanisms linking the tumor microenvironment (TME) and metabolic reprogramming in MASLD-related HCC are not fully elucidated.
  • Chronic inflammation, lipotoxicity, and oxidative stress are key factors in MASLD-associated liver disease progression.

Purpose of the Study:

  • To review the bidirectional crosstalk between TME remodeling and metabolic reprogramming in MASLD-related HCC.
  • To summarize current knowledge on how MASLD influences the TME and metabolic pathways.
  • To highlight the potential of metabolomic profiling for understanding and treating MASLD-related HCC.

Main Methods:

  • Literature review of studies investigating TME remodeling and metabolic reprogramming in MASLD-related HCC.
  • Analysis of key metabolic pathways implicated in liver cancer development.
  • Discussion of emerging metabolomic profiling techniques.

Main Results:

  • Chronic inflammation, lipotoxicity, and oxidative stress significantly alter the TME in MASLD-related HCC.
  • Metabolic reprogramming, including altered immune cell function, creates an immunosuppressive tumor niche.
  • Metabolomic biomarkers derived from TME-metabolic interactions are critical indicators of disease progression and treatment response.

Conclusions:

  • The interplay between TME and metabolism is central to MASLD-related HCC pathogenesis.
  • Metabolomic biomarkers hold significant promise for early diagnosis, disease stratification, and personalized treatment strategies.
  • Targeting TME-metabolic crosstalk offers a promising avenue for advancing precision medicine in MASLD-related HCC.
Keywords:
MASLD-HCChepatocellular carcinomametabolic dysfunction-associated steatotic liver diseasemetabolomicstumor microenvironment

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