Identification of FAM107A as a potential biomarker and therapeutic target for prostate carcinoma

• Published in: American journal of translational research Vol. 13; no. 9; pp. 10163 - 10177
• Main Authors: Ma, Yun-Fei, Li, Guang-Da, Sun, Xu, Li, Xiao-Xiao, Gao, Yu, Gao, Chong, Cao, Ke-Xin, Yang, Guo-Wang, Yu, Ming-Wei, Wang, Xiao-Min
• Format: Journal Article
• Language: English
• Published: e-Century Publishing Corporation 01.01.2021
• Subjects: Original
• ISSN: 1943-8141; 1943-8141

FAM107A may have a dual role in regulating the biological functions of tumors; however, its role in prostate adenocarcinoma (PRAD) remains unknown. We analyzed FAM107A expression by employing databases to clarify its potential prognostic value for PRAD, as well as its role in the pathogenesis of PRAD. We observed that the FAM107A expression level is decreased in PRAD, and the reduced expression is considerably associated with poor overall survival and progression-free survival (PFS). To explore the mechanism of FAN107A in PRAD, we performed an immune cell infiltration analysis and a gene set enrichment analysis. The results showed that FAM107A expression is positively related to mast cells and natural killer cells. The Wnt signaling pathway, the MAPK signaling pathway, and the immune responses are differentially enriched in the FAM107A high-expression phenotype. The FAM107A low-expression phenotype is linked to apoptosis-induced DNA fragmentation and DNA methylation in PRAD. To assess the relationship between the clinical features and the FAM107A expression, we performed a logistic regression analysis and observed that a decreased FAM107A expression is associated with poor prognostic features, including the T stage, the N stage, the Gleason score, residual tumors, and the TP53 status. Our multivariate Cox regression results showed that the Gleason score, the primary therapy outcome, and the FAM107A expression are independent prognostic factors in PFS. In summary, we consider FAM107A an independent risk factor for PFS in PRAD. Moreover, several pathways may reveal the role of FAM107A in triggering carcinogenesis. These discoveries provide novel perspectives for future research to elucidate the pathogenic mechanism underlying PRAD.