1. High expression of centromere protein A and its molecular mechanism and clinical significance in prostate cancer: A study based on data mining and immunohistochemistry.
- Author
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Jiang FC, Zhai GQ, Liu JL, Wang RG, Yang YP, Murugesan H, Yu XX, Du XF, He J, Feng ZB, Pan SL, Chen G, Li SH, and Huang ZG
- Subjects
- Male, Humans, Centromere Protein A genetics, Centromere Protein A metabolism, Immunohistochemistry, Receptors, Androgen genetics, Receptors, Androgen metabolism, Data Mining, Cell Line, Tumor, Gene Expression Regulation, Neoplastic, Clinical Relevance, Prostatic Neoplasms diagnosis, Prostatic Neoplasms genetics, Prostatic Neoplasms metabolism
- Abstract
The progression of prostate cancer (PCa) leads to poor prognosis. However, the molecular mechanism of PCa is still not completely clear. This study aimed to elucidate the important role of centromere protein A (CENPA) in PCa. Large numbers of bulk RNA sequencing (RNA-seq) data and in-house immunohistochemistry data were used in analysing the expression level of CENPA in PCa and metastatic PCa (MPCa). Single-cell RNA-seq data was used to explore the expression status of CENPA in different prostate subpopulations. Enrichment analysis was employed to detect the function of CENPA in PCa. Clinicopathological parameters analysis was utilised in analysing the clinical value of CENPA. The results showed that CENPA was upregulated in PCa (standardised mean difference [SMD] = 0.83, p = 0.001) and MPCa (SMD = 0.61, p = 0.029). CENPA was overexpressed in prostate cancer stem cells (CSCs) with androgen receptor (AR) negative compared to epithelial cells with AR positive. CENPA may influence the development of PCa through affecting cell cycle. Patients with nodal metastasis had higher expression level of CENPA. And patients with high CENPA expression had poor disease-free survival. Taken together, Overexpression of CENPA may influence the development of PCa by regulating cell cycle and promoting metastasis., (© 2023 The Authors. IET Systems Biology published by John Wiley & Sons Ltd on behalf of The Institution of Engineering and Technology.)
- Published
- 2023
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