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3DCity-LLM: Empowering Multi-modality Large Language Models for 3D City-scale Perception and Understanding

arXiv:2603.23447v1 Announce Type: cross Abstract: While multi-modality large language models excel in object-centric or indoor scenarios, scaling them to 3D city-scale environments remains a formidable challenge. To bridge this gap, we propose 3DCity-LLM, a unified framework designed for 3D city-scale vision-language perception and understanding. 3DCity-LLM employs a coarse-to-fine feature encoding strategy comprising three parallel branches for target object, inter-object relationship, and global scene. To facilitate large-scale training, we introduce 3DCity-LLM-1.2M dataset that comprises approximately 1.2 million high-quality samples across seven representative task categories, ranging from fine-grained object analysis to multi-faceted scene planning. This strictly quality-controlled dataset integrates explicit 3D numerical information and diverse user-oriented simulations, enriching the question-answering diversity and realism of urban scenarios. Furthermore, we apply a multi-dimensional protocol based on text-similarity metrics and LLM-based semantic assessment to ensure faithful and comprehensive evaluations for all methods. Extensive experiments on two benchmarks demonstrate that 3DCity-LLM significantly outperforms existing state-of-the-art methods, offering a promising and meaningful direction for advancing spatial reasoning and urban intelligence. The source code and dataset are available at https://github.com/SYSU-3DSTAILab/3D-City-LLM.
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SIRT3 deacetylates STEAP4 to modulate cuproptosis sensitivity via mitochondrial metabolic reprogramming in HBV-related HCC

Cell Death Differ. 2026 Mar 16. doi: 10.1038/s41418-026-01713-w. Online ahead of print.

ABSTRACT

Hepatitis B virus (HBV) infection remains a leading etiological driver of hepatocellular carcinoma (HCC). Cuproptosis is a recently defined copper-dependent form of regulated cell death that selectively eliminates mitochondria-dependent cells; whether HBV rewires this vulnerability remains unknown. Here we unveil a novel HBV X protein (HBx)-driven mechanism of cuproptosis evasion. Integrative analysis of clinical specimens, HBx-transgenic (HBx-Tg) mice, and multi-omics datasets revealed marked downregulation of STEAP4 (six-transmembrane epithelial antigen of prostate 4), a metalloreductase essential for cuproptosis sensitivity, in HBV-positive HCC. Mechanistically, HBx attenuates sirtuin 3 (SIRT3), impairing deacetylation of STEAP4 at lysine 404 and abolishing its mitochondrial targeting. Consequently, cells switch from the tricarboxylic acid (TCA) cycle respiration to glycolysis, reducing sensitivity to the copper ionophore elesclomol (ES). Restoring STEAP4 expression or pharmacological activation of SIRT3 with honokiol (HKL) re-instated mitochondrial STEAP4 localization and re-sensitized HBV-related HCC cells to cuproptosis; combination with ES produced synergistic tumor suppression in vitro and in orthotopic models. Collectively, our findings establish the SIRT3-STEAP4 axis as a novel regulator of cuproptosis resistance in HBV-related HCC. HBx-mediated repression of SIRT3 disrupts STEAP4 deacetylation and mitochondrial targeting, fostering metabolic reprogramming and evasion of copper-induced cell death. The results provide a pre-clinical rationale for copper-directed combination strategies in HBV-associated HCC.

PMID:41840161 | DOI:10.1038/s41418-026-01713-w

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