ArticleOncology research2025
COPB2 promotes hepatocellular carcinoma progression through regulation of YAP1 nuclear translocation.
Article in Oncology research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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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Who cites it
4 citing papers in PubMed.
- COPG1 Is a Selectively Essential Regulator of Cancer Progression and Chemoresistance via Redox Modulation and AKT Signaling.International journal of molecular sciences · 2026Article
- Molecular Subtyping Based on EGFR Mutation-Associated Genes and the Prognostic Role of TRAF2 in Lung Adenocarcinoma.Human mutation · 2026Article
- COPB2 facilitates EDEM3-mediated mannose trimming to sustain ER homeostasis in ovarian cancer.Cellular oncology (Dordrecht, Netherlands) · 2025Article
- The Role of MAPK12 in Prognosis of Patients With Liver Cancer and Effects on Stemness Characteristics.Stem cells international · 2025Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: Although Yes-associated protein 1 (YAP1) is an important oncogene in hepatocellular carcinoma (HCC) progression, its nuclear localization prevents it from being considered a potential therapeutic target. Recently, studies have reported that coatomer protein complex subunit beta 2 (COPB2) also plays a critical role in HCC development; however its mechanism of action is unclear. This study aimed to investigate the role of COPB2 and YAP1 in the progression of HCC and to elucidate the underlying mechanisms. Methods: COPB2 and YAP1 expression in HCC tissues were first analyzed by database searches and immunohistochemistry. Nomogram and artificial neural network models were established based on COPB2 and YAP1 expression. Cell proliferation was detected by cell counting kit-8 and clone formation assay, while cell migration and invasion were assessed using Transwell assays. Finally, the potential mechanisms underlying COPB2 regulation of YAP1 nuclear translocation were explored by immunofluorescence assay and Western blot. Results: COPB2 combined with YAP1 expression was associated with overall postoperative survival in HCC patients and was an independent prognostic factor. High expression of both COPB2 and YAP1 in patients may reduce the efficacy of postoperative transarterial chemoembolization therapy. Conclusions: Our findings suggest that COPB2/YAP1 affects the drug sensitivity of HCC cells to DDP and that targeting COPB2/YAP1 may be a promising strategy for the precision treatment of HCC.
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