ArticleBiochemical and biophysical research communications2014
TLE1 promotes EMT in A549 lung cancer cells through suppression of E-cadherin.
Article in Biochemical and biophysical research communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 48 citations in OpenAlex.
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- Single cell transcriptomic analysis reveals tumor immune infiltration by macrophage cells gene signature in lung adenocarcinoma.Discover oncology · 2025Article
- TLE1 corepressor promotes gefitinib resistance in lung cancer A549 cells via E‑cadherin silencing.Biomedical reports · 2025Article
- Construction and validation of a prognostic model for stemness-related genes in lung adenocarcinoma.Translational cancer research · 2024Article
- Phenethyl isothiocyanate inhibits metastasis potential of non-small cell lung cancer cells through FTO mediated TLE1 mActa pharmacologica Sinica · 2024Article
- RSV-induced expanded ciliated cells contribute to bronchial wall thickening.Virus research · 2023Article
- Elaboration and validation of a prognostic signature associated with disulfidoptosis in lung adenocarcinoma, consolidated with integration of single-cell RNA sequencing and bulk RNA sequencing techniques.Frontiers in immunology · 2023Article
- Regulation of epithelial-mesenchymal transition by protein lysine acetylation.Cell communication and signaling : CCS · 2022Review
- Development of a 5-Gene Signature to Evaluate Lung Adenocarcinoma Prognosis Based on the Features of Cancer Stem Cells.BioMed research international · 2022Article
- Roles of transducin-like enhancer of split (TLE) family proteins in tumorigenesis and immune regulation.Frontiers in cell and developmental biology · 2022Review
- The prognostic role of the Transducin-like Enhancer of split protein family in lung adenocarcinoma.Translational lung cancer research · 2021Article
- KRAS and EGFR Mutations Differentially Alter ABC Drug Transporter Expression in Cisplatin-Resistant Non-Small Cell Lung Cancer.International journal of molecular sciences · 2021Article
- Prognostic Value of TLE1 Gene Expression in Patients with T-cell Acute Lymphoblastic Leukemia.Asian Pacific journal of cancer prevention : APJCP · 2021Article
- Gene signature based on B cell predicts clinical outcome of radiotherapy and immunotherapy for patients with lung adenocarcinoma.Cancer medicine · 2020Article
- Advantages of Restoring miR-205-3p Expression for Better Prognosis of Gastric Cancer via Prevention of Epithelial-mesenchymal Transition.Journal of gastric cancer · 2020Article
- Resveratrol Suppresses Prostate Cancer Epithelial Cell Scatter/Invasion by Targeting Inhibition of Hepatocyte Growth Factor (HGF) Secretion by Prostate Stromal Cells and Upregulation of E-cadherin by Prostate Cancer Epithelial Cells.International journal of molecular sciences · 2020Article
- A Genome-Wide Association Study in Early COPD: Identification of One Major Susceptibility Loci.International journal of chronic obstructive pulmonary disease · 2020Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The Groucho transcriptional corepressor TLE1 protein has recently been shown to be a putative lung specific oncogene, but its underlying oncogenic activity in lung cancer has not been fully elucidated. In this report, we investigated whether TLE1 regulates lung cancer aggressiveness using the human lung adenocarcinoma cell line A549 as a model system. Through a combination of genetic approaches, we found that TLE1 potentiates epithelial-to-mesenchymal transition (EMT) in A549 cells in part through suppression of the tumor suppressor gene E-cadherin. Exogenous expression of TLE1 in A549 cells resulted in heightened EMT phenotypes (enhanced fibroblastoid morphology and increased cell migratory potential) and in molecular alterations characteristic of EMT (downregulation of the epithelial marker E-cadherin and upregulation of the mesenchymal marker Vimentin). Conversely, downregulation of endogenous TLE1 expression in these cells resulted in reversal of basal EMT characterized by a cuboidal-like epithelial cell phenotype, reduced cell motility, and upregulated E-cadherin expression. Mechanistic studies showed that TLE1 suppresses E-cadherin expression at the transcriptional level in part by recruiting histone deacetylase (HDAC) activity to the E-cadherin promoter. Consistently, the HDAC inhibitor TSA partially reversed the TLE1-induced E-cadherin downregulation and cell migration, suggesting a role for HDACs in TLE1-mediated transcriptional repression of E-cadherin and EMT function. These findings uncover a novel role of TLE1 in regulating EMT in A549 cells through its repressive effect on E-cadherin and provide a mechanism for TLE1 oncogenic activity in lung cancer.
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