ArticleOncology research2025
CEP55 Promotes Acral Melanoma Progression via MAPK Pathway and Predicts Survival Following Immunotherapy.
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 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.
- BRAF inhibitor resistance in melanoma: from resistance mechanisms to therapeutic innovations.Molecular biomedicine · 2026Review
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Acral melanoma (AM) is the predominant subtype of cutaneous melanoma in Asian populations, characterized by more aggressive clinical features and limited neoadjuvant therapy response. Centrosomal protein 55 kDa (CEP55) has been implicated in the pathogenesis of various malignancies, but its role in AM remains undefined. Methods: CEP55 expression in melanoma tissues and cell lines was analyzed by RT-qPCR, Western blotting, and immunohistochemistry (IHC). Databases (GEPIA, Sangerbox, Kaplan-Meier plotter, and TIMER) were used to analyze the expression of CEP55 and its correlation with clinical data of melanoma patients. Functional assays were conducted Results: CEP55 overexpression is associated with Breslow thickness and TNM stage in melanoma tissues and cell lines. CEP55 knockdown inhibited melanoma cell proliferation, migration, and invasion. And CEP55 activated mitogen-activated protein kinase (MAPK) signaling, leading to BRAF inhibitor resistance. Besides, CEP55 overexpression was associated with more favorable responses to immunotherapy in melanoma patients. Conclusions: CEP55 plays a critical role in AM progression and immunotherapy. Targeting CEP55 may be a promising therapeutic strategy for AM.
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