ArticleCancer science2025
HROB Induces Lung Adenocarcinoma Progression via ZC3HC1-CCNB1 Axis Regulation and Cell Cycle Dysregulation.
Article in Cancer science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Unveiling DEFB1 as a novel driver and promising therapeutic target in lung adenocarcinoma.Cell death & disease · 2026Article
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Authors and funding
13 authors.
Funding
Abstract
Lung adenocarcinoma (LUAD), a leading cause of cancer-related mortality, remains a significant global health challenge due to limited understanding of its molecular mechanisms. HROB, a recently identified gene, has been implicated in cell cycle regulation, but its role in lung cancer progression is poorly understood. In this study, we demonstrate that HROB suppresses LUAD progression by interacting with ZC3HC1 and reducing its phosphorylation at Ser354. This de-phosphorylation event facilitates K27-linked ubiquitination of CCNB1, promoting its proteasomal degradation and impairing the G2-to-M phase transition. Consequently, HROB suppresses cell proliferation and tumor growth. Our findings reveal a novel HROB-ZC3HC1-CCNB1 regulatory axis, providing mechanistic insights into LUAD progression. These results highlight HROB as a potential therapeutic target, offering new avenues for clinical intervention in lung cancer treatment.
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