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CENPA promotes clear cell renal cell carcinoma progression and metastasis via Wnt/β-catenin signaling pathway

Clear cell renal cell carcinoma (ccRCC) is the most common malignant tumor of the kidney. New and reliable biomarkers are in urgent need for ccRCC diagnosis and prognosis. The CENP family is overexpressed in many types of cancers, but its functions in ccRCC have not been fully clarified. In this pap...

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Detalles Bibliográficos
Autores principales: Wang, Qi, Xu, Jiaju, Xiong, Zhiyong, Xu, Tianbo, Liu, Jingchong, Liu, Yuenan, Chen, Jiaping, Shi, Jian, Shou, Yi, Yue, Changjie, Liu, Di, Liang, Huageng, Yang, Hongmei, Yang, Xiong, Zhang, Xiaoping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8502268/
https://www.ncbi.nlm.nih.gov/pubmed/34627268
http://dx.doi.org/10.1186/s12967-021-03087-8
Descripción
Sumario:Clear cell renal cell carcinoma (ccRCC) is the most common malignant tumor of the kidney. New and reliable biomarkers are in urgent need for ccRCC diagnosis and prognosis. The CENP family is overexpressed in many types of cancers, but its functions in ccRCC have not been fully clarified. In this paper, we found that several CENP family members were highly expressed in ccRCC tissues. Also, CENPA expression level was related to clinicopathological grade and prognosis by weighted gene co-expression network analysis (WGCNA). CENPA served as a representative CENP family member as a ccRCC biomarker. Further in vitro experiments verified that overexpression of CENPA promoted ccRCC proliferation and metastasis by accelerating the cell cycle and activating the Wnt/β-catenin signaling pathway. The elevated β-catenin led by CENPA overexpression translocated to nucleus for downstream effect. Functional recovery experiment confirmed that Wnt/β-catenin pathway was essential for ccRCC progression and metastasis. Developing selective drugs targeting CENPA may be a promising direction for cancer treatment. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12967-021-03087-8.