ArticleCell death & disease2013
TGF-β1 exposure induces epithelial to mesenchymal transition both in CSCs and non-CSCs of the A549 cell line, leading to an increase of migration ability in the CD133+ A549 cell fraction.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 130 citations in OpenAlex.
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- Persistent lineage plasticity driving lung cancer development and progression.Clinical and translational medicine · 2025Review
- SMAD2 linker phosphorylation impacts overall survival, proliferation, TGFβ1-dependent gene expression and pluripotency-related proteins in NSCLC.British journal of cancer · 2025Article
- Non-small cell lung cancer map and analysis: exploring interconnected oncogenic signal integrators.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- The role and clinical significance of tumor-associated macrophages in the epithelial-mesenchymal transition of lung cancer.Frontiers in oncology · 2025Review
- Construction and validation of a prognostic model based on oxidative stress-related genes in non-small cell lung cancer (NSCLC): predicting patient outcomes and therapy responses.Translational lung cancer research · 2024Article
- Elevated expression levels of the protein kinase DYRK1B induce mesenchymal features in A549 lung cancer cells.BMC cancer · 2024Article
- Electrical Impedance Spectroscopy as a Tool to Detect the Epithelial to Mesenchymal Transition in Prostate Cancer Cells.Biosensors · 2024Article
- Mapping cellular interactions from spatially resolved transcriptomics data.Nature methods · 2024Article
- Mantis: High-throughput 4D imaging and analysis of the molecular and physical architecture of cells.PNAS nexus · 2024Article
- Mantis: high-throughput 4D imaging and analysis of the molecular and physical architecture of cells.bioRxiv : the preprint server for biology · 2024Article
- Interstitial flow potentiates TGF-β/Smad-signaling activity in lung cancer spheroids in a 3D-microfluidic chip.Lab on a chip · 2024Article
- Can CD133 Be Regarded as a Prognostic Biomarker in Oncology: Pros and Cons.International journal of molecular sciences · 2023Review
- (Very) Small Stem-like Cells in Human Cell Cultures.Cancers · 2023Article
- AKT2-mediated nuclear deformation leads to genome instability during epithelial-mesenchymal transition.iScience · 2023Article
- Anti-TGF-β1 aptamer enhances therapeutic effect of tyrosine kinase inhibitor, gefitinib, on non-small cell lung cancer in xenograft model.Molecular therapy. Nucleic acids · 2022Article
- Review
- Pan-cancer quantitation of epithelial-mesenchymal transition dynamics using parallel reaction monitoring-based targeted proteomics approach.Journal of translational medicine · 2022Article
- Human embryonic mesenchymal lung-conditioned medium promotes differentiation to myofibroblast and loss of stemness phenotype in lung adenocarcinoma cell lines.Journal of experimental & clinical cancer research : CR · 2022Article
18 more citing papers are in PubMed but not listed here.
Corrections and comments
- Expression of concern
Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastasis is the leading cause of death by cancer. Non-small-cell lung cancer (NSCLC) represents nearly 85% of primary malignant lung tumours. Recent researches have demonstrated that epithelial-to-mesenchymal transition (EMT) plays a key role in the early process of metastasis of cancer cells. Transforming growth factor-β1 (TGF-β1) is the major inductor of EMT. The aim of this study is to investigate TGF-β1's effect on cancer stem cells (CSCs) identified as cells positive for CD133, side population (SP) and non-cancer stem cells (non-CSCs) identified as cells negative for CD133, and SP in the A549 cell line. We demonstrate that TGF-β1 induces EMT in both CSC and non-CSC A549 sublines, upregulating the expression of mesenchymal markers such as vimentin and Slug, and downregulating levels of epithelial markers such as e-cadherin and cytokeratins. CSC and non-CSC A549 sublines undergoing EMT show a strong migration and strong levels of MMP9 except for the CD133(-) cell fraction. OCT4 levels are strongly upregulated in all cell fractions except CD133(-) cells. On the contrary, wound size reveals that TGF-β1 enhances motility in wild-type A549 as well as CD133(+) and SP(+) cells. For CD133(-) and SP(-) cells, TGF-β1 exposure does not change the motility. Finally, assessment of growth kinetics reveals major colony-forming efficiency in CD133(+) A549 cells. In particular, SP(+) and SP(-) A549 cells show more efficiency to form colonies than untreated corresponding cells, while for CD133(-) cells no change in colony number was observable after TGF-β1 exposure. We conclude that it is possible to highlight different cell subpopulations with different grades of stemness. Each population seems to be involved in different biological mechanisms such as stemness maintenance, tumorigenicity, invasion and migration.
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