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The role of HNF4α in adenocarcinoma
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DOI：10.1042/BST20253085.png)
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Abstract
En 中文
Hepatocyte nuclear factor 4 alpha (HNF4 alpha) is a conserved nuclear receptor that governs epithelial identity and metabolic homeostasis across endoderm-derived tissues. In cancer, HNF4 alpha can function as either an oncogene or a tumor suppressor. In colorectal and hepatocellular carcinoma, reduced HNF4 alpha activity accompanies loss of differentiation and tumor progression, consistent with tumor-suppressive functions. In contrast, in pancreatic ductal adenocarcinoma, invasive mucinous adenocarcinoma, and other lineage-defined epithelial tumors, HNF4 alpha can also participate in transcriptional programs that sustain malignant identity, metabolic adaptation, and therapeutic resistance. However, these effects are highly context-dependent and do not imply a uniformly oncogenic role in these tumor types. These divergent functions are shaped by isoform usage, chromatin state, epigenetic regulation, metabolic cues, and transcription factor networks. Rather than acting as a classical oncogene or tumor suppressor in all settings, HNF4 alpha is better understood as a context-dependent regulator of lineage state whose activity may either restrain tumor progression or support tumor maintenance. This mini review highlights the molecular mechanisms that shape HNF4 alpha activity, including isoform biology and epigenetic control, and discusses emerging strategies for selectively inhibiting HNF4 alpha in dependency states or restoring its differentiation-promoting functions in tumors where it is lost.
Keywords:
NUCLEAR FACTOR 4-ALPHA
INVASIVE MUCINOUS ADENOCARCINOMA
TRANSCRIPTION FACTOR
GASTRIC-CANCER
HEPATOCYTE PROLIFERATION
TUMOR PROGRESSION
IMPROVED SURVIVAL
4 ALPHA
EXPRESSION
LIVER
Journal
B
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