Wu Jie, Chen Yang, Yang Xiaoqi, Kuang Huabing, Feng Ting, Deng Chengmin, Li Xiaoqian, Ye Meng, Tan Xin, Gong Ling, Wang Ya, Shen Yuguang, Qu Jingqiu, Wu Kaifeng
Scientific Research Center, The Third Affiliated Hospital of Zunyi Medical University (The First People's Hospital of Zunyi), Zunyi, Guizhou, China.
Scientific Research Center, The Third Affiliated Hospital of Zunyi Medical University (The First People's Hospital of Zunyi), Zunyi, Guizhou, China; College of Basic Medicine, Zunyi Medical University, Zunyi, Guizhou, China.
Gene. 2025 Mar 10;940:149199. doi: 10.1016/j.gene.2024.149199. Epub 2024 Dec 26.
Pre-existing of pulmonary tuberculosis (PTB) poses increased lung cancer risk, yet the molecular mechanisms remain inadequately understood. This study sought to elucidate the potential mechanisms by performing comprehensive analyses of differentially expressed genes (DEGs) in peripheral blood mononuclear cells (PBMCs) from patients with PTB, lung adenocarcinoma (LUAD), and lung squamous cell carcinoma (LUSC). Microarray assays were employed to analyze the DEGs in PBMCs of these patients. The analyses revealed that, compared to healthy controls, the number of differentially expressed LncRNA in PBMCs from patients with PTB, LUAD, and LUSC were 801, 8,541, and 7,796, respectively. Similarly, the differentially expressed mRNA in PBMCs from patients with PTB, LUAD, and LUSC were 629, 4,865, and 4,438, respectively. These differentially expressed transcripts represent significant resources for the identifying diagnostic and differential diagnostic biomarkers for lung cancer and PTB. Pathways enriched by dysregulated mRNAs in patients with PTB, LUAD, and LUSC were identified through GO and KEGG pathway analyses. The results indicated that 9 pathways including the NOD-like receptor signaling pathway, pathways in cancer, and the MAPK signaling pathway were co-enriched across the PTB, LUAD, and LUSC groups, providing insights into the mechanisms by which PTB may increase the risk of cancer development and progression.
既往存在肺结核（PTB）会增加肺癌风险，但其分子机制仍未得到充分了解。本研究旨在通过对肺结核患者、肺腺癌（LUAD）患者和肺鳞状细胞癌（LUSC）患者外周血单个核细胞（PBMC）中的差异表达基因（DEG）进行综合分析，阐明潜在机制。采用微阵列分析来检测这些患者PBMC中的DEG。分析显示，与健康对照相比，肺结核患者、肺腺癌患者和肺鳞状细胞癌患者PBMC中差异表达的长链非编码RNA（LncRNA）数量分别为801、8541和7796。同样，肺结核患者、肺腺癌患者和肺鳞状细胞癌患者PBMC中差异表达的信使核糖核酸（mRNA）分别为629、4865和4438。这些差异表达的转录本是识别肺癌和肺结核诊断及鉴别诊断生物标志物的重要资源。通过基因本体（GO）和京都基因与基因组百科全书（KEGG）通路分析，确定了肺结核患者、肺腺癌患者和肺鳞状细胞癌患者中失调mRNA富集的通路。结果表明，包括NOD样受体信号通路（NOD-like receptor signaling pathway）、癌症通路（pathways in cancer）和丝裂原活化蛋白激酶信号通路（MAPK signaling pathway）在内共有9条通路在肺结核、肺腺癌和肺鳞状细胞癌组中共同富集，这为肺结核可能增加癌症发生和进展风险的机制提供了见解。
