ArticleCurrent molecular medicine2024
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.
Article in Current molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 2 citations in OpenAlex.
- OLR1 promotes cell proliferation and invasion while represses apoptosis via regulating histone H3 lysine 18 lactylation‑mediated LEMD1 in papillary thyroid cancer.Oncology reports · 2026Article
- Advances in the molecular mechanisms and clinical applications of LEMD1 in tumor development and progression (Review).Molecular and clinical oncology · 2026Review
- Nuclear envelope proteins in cancer: revisiting the significance of LEM-domain proteins.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNon-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.
objectiveThis study aimed to investigate the LEMD1 function in NSCLC.
methodsNSCLC 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
resultsLEMD1 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
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