ArticleBioengineered2022
LEM domain containing 1 promotes pancreatic cancer growth and metastasis by p53 and mTORC1 signaling pathway.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 6 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
- CENPN contributes to pancreatic carcinoma progression through the MDM2-mediated p53 signaling pathway.Archives of medical science : AMS · 2024Article
- 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.Current molecular medicine · 2024Article
- LEM Domain Containing 1 Acts as a Novel Oncogene and Therapeutic Target for Triple-Negative Breast Cancer.Cancers · 2023Article
- SLC8A1 antisense RNA 1 suppresses papillary thyroid cancer malignant progression via the FUS RNA binding protein (FUS)/NUMB like endocytic adaptor protein (Numbl) axis.Bioengineered · 2022Article
- Network Pharmacology-Integrated Molecular Docking Reveals the Expected Anticancer Mechanism ofBioMed research international · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pancreatic cancer (PC) is a common type of malignancy originating from the epithelium of the pancreatic duct, with the most lethal feature and worst prognosis. LEM domain containing 1 (LEMD1) is overexpressed in multiple tumor tissues and plays a key role in cancer carcinogenesis and progression. However, little is known about the potential of LEMD1 in PC. In this study, we explored the clinical values, as well as the potential roles and mechanisms of LEMD1 in PC. We, for the first time, showed that LEMD1 was upregulated in PC and negatively correlated with the overall and disease-free survival of patients with PC. Of the function, LEMD1 knockdown inhibited cancer cell growth, migration and invasion, while LEMD1 overexpression promoted tumor aggressiveness. The tumor-promoting influences of LEMD1 in PC were also proved by in vivo assays. Mechanistically, GSEA identified that LEMD1 promoted PC aggressiveness, as well as affecting cell cycle dysregulation and apoptosis resistance, by p53 suppression and the activation of the mTORC1 signal pathway. In short, LEMD1 could serve as a valuable prognostic candidate and a potential therapeutic target of PC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.