HBx Downregulates TFEB via the CUL4A/CUL4B-DDB1 Axis to Disrupt Lysosomal Function in Hepatocellular Carcinoma Cells.

Chunyan Zhang, Yuanping Han, Huan Yang

Abstract read

In one paragraph

Article in Cells, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed

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1 · What the graph read from it

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Chunyan ZhangSchool of Basic Medicine, Shaanxi University of Chinese Medicine, Xianyang 712046, China.

Yuanping HanThe Center for Growth, Metabolism and Aging, College of Life Sciences, Sichuan University, Chengdu 610065, China.ORCID 0000-0001-6282-7319

Huan YangThe Center for Growth, Metabolism and Aging, College of Life Sciences, Sichuan University, Chengdu 610065, China.

Funding

Key Research and Development Program of Xianyang L2024-ZDYF-ZDYF-SF-0043Qinchuangyuan Traditional Chinese Medicine Industry Innovation Cluster Project L2024-QCY-ZYYJJQ-X152

6 · The paper itself

Abstract

Hepatitis B virus (HBV) infection remains a major global health burden, with chronic infection leading to severe liver diseases including cirrhosis and hepatocellular carcinoma (HCC). HBV-encoded X protein (HBx) plays a critical role in viral replication and pathogenesis by modulating host cellular processes, including autophagy and lysosomal function. However, the molecular mechanisms by which HBx disrupts lysosomal biogenesis and autophagic degradation remain elusive. In this study, we show that HBx downregulates the transcription factor EB (TFEB), a master regulator of lysosomal biogenesis, which leading to impaired lysosomal acidification and autophagosome-lysosome fusion. Mechanistically, HBx-mediated TFEB downregulation involves the CUL4A (Cullin 4A)/CUL4B (Cullin 4B)-DDB1 (DNA damage-binding protein 1) E3 ubiquitin ligase complex and is dependent on the DDB1-interacting motif in HBx. HBx mutants defective in DDB1 binding (HBx

Indexed as

Basic Helix-Loop-Helix Leucine Zipper Transcription FactorsCarcinoma, HepatocellularCullin ProteinsDNA-Binding ProteinsDown-RegulationLiver NeoplasmsLysosomesTrans-ActivatorsViral Regulatory and Accessory ProteinsCell Line, TumorHepatitis B virusHep G2 CellsHumansBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCUL4A protein, humanCUL4B protein, humanCullin ProteinsDDB1 protein, humanDNA-Binding Proteinshepatitis B virus X proteinTFEB protein, humanTrans-ActivatorsViral Regulatory and Accessory ProteinsCUL4A/CUL4BHBxhepatocellular carcinomalysosomeTFEB

Identifiers

PMID42505369

DOI10.3390/cells15141259

PMCPMC13406449

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.