Title: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
Volume: 24
Issue: 3
Author(s): Li Li and Pei Zhang*
Affiliation:
- Department of Cardiothoracic Surgery, The Second Affiliated Hospital of Chongqing Medical University,
Chongqing, 402177, China
Keywords:
LEMD1, NSCLC, proliferation, PI3K/AKT, PCR, TNM stage
Abstract:
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.
