Open Access

ARTICLE

CEP55 Promotes Acral Melanoma Progression via MAPK Pathway and Predicts Survival Following Immunotherapy

Meng Cao, Rundong Zhang, Anlan Hong, Shanyuan Ye, Zequn Qiu, Dongqing Li, Tong Lin^*, Yan Wang^*

Hospital for Skin Diseases, Institute of Dermatology, Chinese Academy of Medical Sciences & Peking Union Medical College, Nanjing, 210042, China

* Corresponding Authors: Tong Lin. Email: ; Yan Wang. Email:

(This article belongs to the Special Issue: Signaling Pathway Crosstalk in Malignant Tumors: Molecular Targets and Combinatorial Therapeutics)

Oncology Research 2025, 33(9), 2507-2527. https://doi.org/10.32604/or.2025.064780

Received 24 February 2025; Accepted 06 May 2025; Issue published 28 August 2025

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 in vitro and in vivo. RNA sequencing (RNA-seq) and rescue experiments were used to explore underlying mechanisms. Tissue microarrays were used to verify the relationship between CEP55 and immune checkpoints. 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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