Elevation of LEM Domain Containing 1 Predicts Poor Prognosis of NSCLC Patients and Triggers Malignant Stemness and Invasion of NSCLC Cells by Stimulating PI3K/AKT Pathway

作者全名："Li, Li; Zhang, Pei"

作者地址："[Li, Li; Zhang, Pei] Chongqing Med Univ, Dept Cardiothorac Surg, Affiliated Hosp 2, Chongqing 402177, Peoples R China; [Zhang, Pei] Chongqing Med Univ, Dept Cardiothorac Surg, Affiliated Hosp 2, 76 Linjiang Rd, Chongqing 402177, Peoples R China"

通信作者："Zhang, P (通讯作者)，Chongqing Med Univ, Dept Cardiothorac Surg, Affiliated Hosp 2, 76 Linjiang Rd, Chongqing 402177, Peoples R China."

来源：CURRENT MOLECULAR MEDICINE

ESI学科分类：CLINICAL MEDICINE

WOS号：WOS:001185306400007

JCR分区：Q3

影响因子：2.2

年份：2024

卷号：24

期号：3

开始页：366

结束页：378

文献类型：Article

关键词：LEMD1; NSCLC; proliferation; PI3K/AKT; PCR; TNM stage

摘要："Background Non-small cell lung cancer (NSCLC) is a leading cause of cancer-related death globally. LEM domain containing 1 (LEMD1) function has been identified in several cancers but not in NSCLC.Objective This study aimed to investigate the LEMD1 function in NSCLC.Methods NSCLC tissues were obtained from 66 patients, and LEMD1 expressions were measured using quantitative real-time PCR, immunohistochemical assay, and Western blot. Overall survival of NSCLC patients was estimated by the Kaplan-Meier method. Meanwhile, LEMD1 function and mechanism were assessed using Cell Counting Kit-8, 5-Ethynyl-2 '-deoxyuridine analysis, Transwell, Sphere formation assay, and flow cytometry. Furthermore, LEMD1 function in vivo was evaluated by establishing a xenograft tumor model, hematoxylin-eosin staining, and immunohistochemical assay.Results LEMD1 was highly expressed in NSCLC tissues and was interrelated to tumor differentiation, TNM stage, and lymph node metastasis of patients. Overall survival of NSCLC patients with high LEMD1 was found to be lower than that of patients with low LEMD1. Functionally, interference with LEMD1 restrained NSCLC cell proliferation, invasion, and stemness characteristics. Mechanistically, LEMD1 facilitated the malignant phenotype of NSCLC, and 740 Y-P reversed this impact, prompting that LEMD1 aggravated NSCLC by activating PI3K/AKT pathway. Furthermore, LEMD1 knockdown hindered NSCLC proliferation in vivo.Conclusion LEMD1 accelerated NSCLC cell proliferation, invasion, and stemness characteristics via activating PI3K/AKT pathway."

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