Bioinformatics analysis and validation of CSRNP1 as a key prognostic gene in non-small cell lung cancer

被引:0
|
作者
Xu, Zhongneng [1 ]
Zhou, Hao [2 ]
Luo, Yonggang [1 ]
Li, Nunu [3 ]
Chen, Sheng [1 ]
机构
[1] Nanjing Med Univ, Dept Thorac Surg, Affiliated Huaian Peoples Hosp 1, 6 West Beijing Rd, Huaian 223300, Jiangsu, Peoples R China
[2] Guanyun Peoples Hosp, Dept Thorac Surg, Guanyun 222299, Sichuan, Peoples R China
[3] AF Hlth Care Ctr Special Serv Hangzhou Sanat 5, Dept Sanat 1, Hangzhou 310002, Zhejiang, Peoples R China
关键词
Non -small cell lung cancer; CSRNP1; Tumor tissues; Survival; Biological mechanism; SIGNALING PATHWAY; CYCLE ARREST; P53; EXPRESSION; MDM2; IDENTIFICATION; PROLIFERATION; EPIDEMIOLOGY; COMBINATION; STATISTICS;
D O I
10.1016/j.heliyon.2024.e28412
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Cysteine and serine-rich nuclear protein 1 (CSRNP1) has shown prognostic significance in various cancers, but its role in non-small cell lung cancer (NSCLC) remains elusive. We investigated CSRNP1 expression in NSCLC cases using bioinformatics tools from the GEO public repository and validated our findings through RT-qPCR in tumor and adjacent normal tissues. KEGG and GO enrichment analyses were employed to unveil the significant deregulation in signaling pathways. Additionally, clinical significance of CSRNP1 in NSCLC was determined through receiver operating curve (ROC) analysis, and its impact on survival was assessed using Kaplan-Meier analysis. To explore the functional impact of CSRNP1, we silenced its expression in NSCLC cells and assessed the effects on cell viability, migration, and invasion using MTT, Transwell, and woundhealing assays, respectively. Additionally, we investigated the influence of CSRNP1 silencing on the phosphorylation patterns of critical signaling proteins such as p53, p-Akt, and p-MDM2. Our results demonstrated significantly lower CSRNP1 expression in NSCLC tumor tissues (P < 0.01). ROC analysis indicated that NSCLC patients with high CSRNP1 expression exhibited extended overall survival and disease-free survival. Furthermore, CSRNP1 silencing promoted NSCLC cells viability, migration, and invasion (P < 0.05). Mechanistically, CSRNP1 silencing led to increased phosphorylation of AKT and MDM2, along with a concurrent reduction in p53 protein expression, suggesting its impact on NSCLC through deregulated cell cycle processes. In conclusion, our study underscores the significance of CSRNP1 in NSCLC pathogenesis, offering insights for targeted therapeutic interventions of NSCLC.
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页数:12
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