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Single-cell RNA sequencing of human hepatocellular carcinoma and adjacent non-tumour liver tissues reveals etiology-associated and etiology-independent tumour microenvironmental features

ABSTRACT: Hepatocellular carcinoma (HCC) arises in the context of diverse aetiological backgrounds, yet the extent to which the tumour microenvironment is shaped by aetiology-associated versus aetiology-independent programmes remains incompletely understood. This dataset was generated to support interrogation of the cellular architecture of human HCC and the surrounding liver microenvironment at single-cell resolution. By profiling tumour and adjacent non-tumour liver tissues, the study provides a resource for examining malignant, immune, stromal, and hepatic parenchymal cell populations, and for investigating shared and aetiology-linked features of the HCC tumour microenvironment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE326201 | GEO | 2026/05/27

REPOSITORIES: GEO

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Project description:Metabolic dysfunction–associated fatty liver disease (MAFLD) can progress to hepatocellular carcinoma (HCC), yet the immune mechanisms driving this transition remain unclear. In a chronic Western diet (WD) mouse model, we performed single-nuclei RNA sequencing to track MAFLD progression into HCC and subsequent tumor inhibition upon dietary correction. Carcinogenesis begins during MAFLD, with tumor cells entering dormancy when HCC is mitigated. Rather than purely tolerogenic, the liver actively engages immune responses targeting myofibroblasts, fibroblasts and hepatocytes to maintain tissue homeostasis. Cytotoxic cells contribute to turnover of liver cells but do not primarily target the tumor. NKT cells predominate under chronic WD, while monocytes join them in HCC progression on a WD. Upon dietary correction, monocyte-driven immunity confers protection against HCC through targeting tissue homeostatic pathways and antioxidant mechanisms. Crucially, liver tissue response—not merely immune activation—dictates whether tumors grow or regress, emphasizing the importance of restoring liver tissue integrity. Also, protection against HCC is linked to a distinct immunological pattern, differing from healthy controls, underscoring the need for immune reprogramming. These findings reveal the dual roles of similar pathways, where immune patterns targeting different cells shape distinct outcomes. Restoring tissue homeostasis and regeneration creates a tumor-hostile microenvironment, whereas tumor-directed approaches fail to remodel the TME. This underscores the need for tissue remodeling strategies in cancer prevention and treatment. Our study challenges the traditional view that the liver is purely tolerant to immune responses, revealing that it actively regulates immunity to maintain tissue health. We found that liver cancer (HCC) begins during fatty liver disease (MAFLD) but can be halted if immune cells—especially monocytes—restore tissue integrity. Instead of focusing solely on killing tumors, effective immunotherapy should harness the body’s natural ability to repair the liver, creating an environment where cancer cannot thrive. This discovery paves the way for innovative treatments that promote immune-driven tissue regeneration as a strategy for cancer prevention and therapy.

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Single-cell RNA sequencing of human hepatocellular carcinoma and adjacent non-tumour liver tissues reveals etiology-associated and etiology-independent tumour microenvironmental features

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