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Abstract：
Lung adenocarcinoma (LUAD), a leading cause of cancer-related mortality worldwide, demands a deeper understanding of its molecular mechanisms and the identification of reliable biomarkers for better diagnosis and targeted therapy. Leveraging data from the Cancer Genome Atlas (TCGA), the Clinical Proteomic Tumor Analysis Consortium (CPTAC), and the Human Protein Atlas (HPA), we investigated the mRNA and protein expression profiles of TIMM17A and assessed its prognostic significance through Kaplan-Meier survival curves and Cox regression analysis. Through Gene Set Enrichment Analysis, we explored the regulatory mechanisms of TIMM17A in LUAD progression and demonstrated its role in modulating the proliferative capacity of A549 cells, a type of LUAD cell, via in vitro experiments. Our results indicate that TIMM17A is significantly upregulated in LUAD tissues, correlating with clinical staging, lymph node metastasis, overall survival, and progression-free survival, thereby establishing it as a critical independent prognostic factor. The construction of a nomogram model further enhances our ability to predict patient outcomes. Knockdown of TIMM17A inhibited the growth of LUAD cells. The potential of TIMM17A as a biomarker and therapeutic target for LUAD presents a promising pathway for improving patient diagnosis and treatment strategies.
摘要：
肺腺癌(LUAD),全球癌症相关死亡的主要原因，需要更深入地了解其分子机制，并确定可靠的生物标志物，以更好地诊断和靶向治疗。利用来自癌症基因组图谱(TCGA)的数据，临床蛋白质组学肿瘤分析联盟（CPTAC），和人类蛋白质图谱（HPA），我们研究了TIMM17A的mRNA和蛋白表达谱,并通过Kaplan-Meier存活曲线和Cox回归分析评估了其预后意义.通过基因集富集分析，我们探索了TIMM17A在LUAD进展中的调控机制，并证明了其在调节A549细胞增殖能力中的作用，一种LUAD细胞,通过体外实验。我们的结果表明，TIMM17A在LUAD组织中显著上调，与临床分期相关，淋巴结转移,总生存率,和无进展生存期，从而将其确立为关键的独立预后因素。列线图模型的构建进一步增强了我们预测患者结果的能力。敲除TIMM17A抑制LUAD细胞的生长。TIMM17A作为LUAD的生物标志物和治疗靶标的潜力为改善患者诊断和治疗策略提供了有希望的途径。
