Department of Medical Laboratory Diagnostics, School of Medical Technology, Shaoyang University, Shaoyang 422000, China.
Department of Family Medicine, Michigan State University, East Lansing, MI 49684, USA.
Int J Mol Sci. 2024 Jul 2;25(13):7290. doi: 10.3390/ijms25137290.
Prostate adenocarcinoma (PRAD) is the second most common tumor associated with death. The role and mechanisms of the fragile X mental retardation 1 () gene in PRAD remain unknown. We conducted an analysis of expression in PRAD to determine its prognostic importance and connection to carcinogenic pathways such as . Survival analyses were utilized to establish a correlation between expression and patient outcomes. We used the integration of genomic data with bioinformatic predictions to predict the regulatory factors of the gene in PRAD. Our data revealed that individuals with higher levels of expression experience worse survival outcomes compared to those with lower expression (hazard ratio [HR] = 5.08, 95% confidence interval [CI] = 1.07 - 24, = 0.0412). expression was significantly higher in patients with advanced pathological tumor stages, particularly in the pT3 and pT4 combined stages and the pN1 nodal stage. Furthermore, patients with high Gleason scores (GSs) (combined GSs 8 and 9) exhibited increased levels of expression. Our results further identify a possible regulatory link between and key oncogenic pathways, including , and predict the possible mechanism by which is regulated in PRAD. Our data suggest that the gene could serve as a biomarker for PRAD progression. However, in-depth investigations, including those with large patient samples and in vitro studies, are needed to validate this finding and understand the mechanisms involved.
前列腺腺癌 (PRAD) 是与死亡相关的第二大常见肿瘤。脆性 X 智力低下 1 号基因 () 在 PRAD 中的作用和机制尚不清楚。我们对 PRAD 中的 表达进行了分析,以确定其预后重要性及其与致癌途径的关系,如 。生存分析用于建立 表达与患者结局之间的相关性。我们利用基因组数据与生物信息学预测的整合来预测 PRAD 中 基因的调节因子。我们的数据表明,与低表达的患者相比,表达水平较高的患者生存结局更差(风险比 [HR] = 5.08,95%置信区间 [CI] = 1.07 - 24,= 0.0412)。在晚期病理肿瘤分期的患者中, 表达水平显著升高,尤其是在 pT3 和 pT4 联合分期和 pN1 淋巴结分期中。此外,具有高 Gleason 评分 (GS)(合并 GSs 8 和 9)的患者 表达水平升高。我们的结果进一步确定了 与关键致癌途径(包括 )之间可能的调节联系,并预测了 在 PRAD 中调节的可能机制。我们的数据表明, 基因可能是 PRAD 进展的生物标志物。然而,需要包括大样本患者和体外研究在内的深入研究来验证这一发现并了解所涉及的机制。