ArticleCell cycle (Georgetown, Tex.)2013
TrkB is responsible for EMT transition in malignant pleural effusions derived cultures from adenocarcinoma of the lung.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- A Meta-Analysis of Human Transcriptomics Data in the Context of Peritoneal Dialysis Identifies Novel Receptor-Ligand Interactions as Potential Therapeutic Targets.International journal of molecular sciences · 2021Pooled it
- Hallmarks of epithelial-mesenchymal plasticity in cancer.Molecular cancer · 2026Review
- Human Wharton's Jelly Mesenchymal Stem Cell Secretome Modifies the Processes of Neuroprotection and Epithelial-Mesenchymal Transition in Retinal Pigment Epithelium at Transcriptional Level.Molecular biology reports · 2023Article
- Adenocarcinomas of the Lung and Neurotrophin System: A Review.Biomedicines · 2022Review
- Review
- Anoikis resistance in diffuse glioma: The potential therapeutic targets in the future.Frontiers in oncology · 2022Review
- TrkB-Targeted Therapy for Mucoepidermoid Carcinoma.Biomedicines · 2020Article
- Immunity against cancer cells may promote their proliferation and metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Full-Length TrkB Variant in NSCLC Is Associated with Brain Metastasis.BioMed research international · 2020Article
- Cancer stem cells-driven tumor growth and immune escape: the Janus face of neurotrophins.Aging · 2019Article
- B4GALT1 Is a New Candidate to Maintain the Stemness of Lung Cancer Stem Cells.Journal of clinical medicine · 2019Article
- Targeting the BDNF/TrkB pathway for the treatment of tumors.Oncology letters · 2019Review
- Promotion of malignant phenotype after disruption of the three-dimensional structure of cultured spheroids from colorectal cancer.Oncotarget · 2018Article
- Article
- BDNF/TrkB axis activation promotes epithelial-mesenchymal transition in idiopathic pulmonary fibrosis.Journal of translational medicine · 2017Article
- Malignant Pleural Effusion and ascites Induce Epithelial-Mesenchymal Transition and Cancer Stem-like Cell Properties via the Vascular Endothelial Growth Factor (VEGF)/Phosphatidylinositol 3-Kinase (PI3K)/Akt/Mechanistic Target of Rapamycin (mTOR) Pathway.The Journal of biological chemistry · 2016Article
- Neurotrophin signaling in cancer stem cells.Cellular and molecular life sciences : CMLS · 2016Review
- Tropomyosin-related kinase B/brain derived-neurotrophic factor signaling pathway as a potential therapeutic target for colorectal cancer.World journal of gastroenterology · 2016Review
- Neurotrophin receptor TrkB promotes lung adenocarcinoma metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- TrkC expression predicts favorable clinical outcome in invasive ductal carcinoma of breast independent of NT-3 expression.American journal of cancer research · 2014Article
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer is the leading cause of cancer-related mortality worldwide. Recent evidence indicates that tumors contain a subpopulation of cancer stem cells (CSCs) that are responsible for tumor maintenance and spread. CSCs have recently been linked to the occurrence of epithelial-to-mesenchymal transition (EMT). Neurotrophins (NTs) are growth factors that regulate the biology of embryonic stem cells and cancer cells, but still little is known about the role NTs in the progression of lung cancer. In this work, we investigated the role of the NTs and their receptors using as a study system primary cell cultures derived from malignant pleural effusions (MPEs) of patients with adenocarcinoma of the lung. We assessed the expression of NTs and their receptors in MPE-derived adherent cultures vs. spheroids enriched in CSC markers. We observed in spheroids a selectively enhanced expression of TrkB, both at the mRNA and protein levels. Both K252a, a known inhibitor of Trk activity, and a siRNA against TrkB strongly affected spheroid morphology, induced anoikis and decreased spheroid forming efficiency. Treatment with neurotrophins reversed the inhibitory effect of K252a. Importantly, TrkB inhibition caused loss of vimentin expression as well as that of a set of transcription factors known to be linked to EMT. These ex vivo results nicely correlated with an inverse relationship between TrkB and E-cadherin expression measured by immunohistochemistry in a panel of lung adenocarcinoma samples. We conclude that TrkB is involved in full acquisition of EMT in lung cancer, and that its inhibition results in a less aggressive phenotype.
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