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FAM111B Acts as an Oncogene in Bladder Cancer

SIMPLE SUMMARY: Bladder cancer can be categorized into non-muscle- and muscle-invasive bladder cancer based on the extent of invasion. While non-muscle-invasive bladder cancer is associated with a low mortality rate, it displays a high recurrence rate, and more than half of the patients are at risk...

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Detalles Bibliográficos
Autores principales: Huang, Ning, Peng, Lei, Yang, Jiaping, Li, Jinqian, Zhang, Sheng, Sun, Mingjuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10648174/
https://www.ncbi.nlm.nih.gov/pubmed/37958297
http://dx.doi.org/10.3390/cancers15215122
Descripción
Sumario:SIMPLE SUMMARY: Bladder cancer can be categorized into non-muscle- and muscle-invasive bladder cancer based on the extent of invasion. While non-muscle-invasive bladder cancer is associated with a low mortality rate, it displays a high recurrence rate, and more than half of the patients are at risk of progressing to muscle-invasive bladder cancer. Traditional treatments, such as surgery and chemotherapy, significantly impact the patients’ quality of life. However, targeted therapies offer potential breakthroughs in the treatment of bladder cancer. Our study identified FAM111B as an oncogene that promotes the tumorigenesis, progression, and metastasis of bladder cancer. Thus, FAM111B gene is expected to serve as a promising molecular target for the therapy of bladder cancer. ABSTRACT: Bladder cancer (BLCA) is a prevalent malignancy of the urinary system, associated with a high recurrence rate and poor prognosis. FAM111B, which encodes a protein containing a trypsin-like cysteine/serine peptidase domain, has been implicated in the progression of various human cancers; however, its involvement in BLCA remains unclear. In this study, we investigated the expression of FAM111B gene in tumor tissues compared to para-tumor tissues using immunohistochemistry and observed a significantly higher FAM111B gene expression in tumor tissues. Furthermore, analysis of clinical characteristics indicated that the increased FAM111B gene expression correlated with lymphatic metastasis and reduced overall survival. To investigate its functional role, we employed FAM111B-knockdown BLCA cell models and performed cell proliferation, wound-healing, transwell, and flow cytometry assays. The results showed that decreased FAM111B gene expression inhibited proliferation and migration but induced apoptosis in BLCA cells. In vivo experiments further validated that FAM111B knockdown suppressed tumor growth. Overall, our findings suggest that FAM111B acts as an oncogene in BLCA, playing a critical role in tumorigenesis, progression, and metastasis of BLCA. In conclusion, we have demonstrated a strong correlation between the expression of FAM111B gene and the development, progression, and metastasis of bladder cancer (BLCA). Thus, FAM111B is an oncogene associated with BLCA and holds promise as a molecular target for future treatment of this cancer.