ArticleJournal of cancer research and clinical oncology2016
Norepinephrine induced epithelial-mesenchymal transition in HT-29 and A549 cells in vitro.
Article in Journal of cancer research and clinical oncology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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Who cites it
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
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- C-MYC as a key effector of WNT, PI3K/AKT, MAPK, and TGF-β signaling pathways in regulation of epithelial-mesenchymal transition during tumor metastasis.Cancer cell international · 2026Review
- Cancer Neoaxonogenesis: Mechanisms and Factors Involved in the Recruitment of Peripheral Nerves by Cancer Tissue.International journal of molecular sciences · 2026Review
- Stress Biology in Cancer: Neuroendocrine-Immune Mechanisms Linking Tumor Progression to Translational Interventions.Cancer communications (London, England) · 2026Review
- Neural regulation of lung cancer: from mechanisms to clinical implications.European journal of medical research · 2025Review
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- Effect of Ritanserin and Duloxetine on the Gene Expression of Primary Aniridia and Healthy Human Limbal Stromal Cells, In Vitro.Ophthalmology and therapy · 2024Article
- Propranolol inhibits EMT and metastasis in breast cancer through miR-499-5p-mediated Sox6.Journal of cancer research and clinical oncology · 2024Article
- Chronic restraint stress promotes oral squamous cell carcinoma development by inhibiting ALDH3A1 via stress response hormone.BMC oral health · 2024Article
- Increased sympathetic nervous system impairs prognosis in lung cancer patients: a scoping review of clinical studies.Lung cancer management · 2023Article
- Effects of norepinephrine‑induced activation of rat vascular adventitial fibroblasts on proliferation and migration of BMSCs involved in vascular remodeling.Experimental and therapeutic medicine · 2023Article
- The neural addiction of cancer.Nature reviews. Cancer · 2023Review
- Effect of chronic stress on tumorigenesis and development.Cellular and molecular life sciences : CMLS · 2022Review
- Targeting HIC1/TGF-β axis-shaped prostate cancer microenvironment restrains its progression.Cell death & disease · 2022Article
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- Interplay between Metabolism Reprogramming and Epithelial-to-Mesenchymal Transition in Cancer Stem Cells.Cancers · 2021Review
- Cancer and Stress: Does It Make a Difference to the Patient When These Two Challenges Collide?Cancers · 2021Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeNorepinephrine (NE) has been implicated in epithelial-mesenchymal transition (EMT) of cancer cells. However, the underlying mechanism is poorly understood. The goal of this study was to explore the effect of NE on cancer cell EMT and to investigate the potential mechanism.
methodsHT-29 and A549 cells were treated with NE, β-adrenergic receptor (β-AR) antagonist (propranolol) or inhibitor of transforming growth factor-β (TGF-β) receptor type I kinase (Ly2157299). Morphology of cells was observed with optical and electron microscope and immunofluorescence staining. Cellular migration and invasion were tested with transwell migration assay and Matrigel invasion assay, respectively. TGF-β1 and cyclic adenosine monophosphate (cAMP) were quantified. EMT markers and signaling pathway were measured by RT-PCR and western blot.
resultsNE stimulated TGF-β1 secretion and intracellular cAMP synthesis, induced morphological alterations in HT-29 and A549 cells, and enhanced their ability of migration and invasion. EMT markers induction was observed in NE-treated cancer cells. The effect of NE could be inhibited by propranolol or Ly2157299. β-AR/TGF-β1 signaling/p-Smad3/Snail and β-AR/TGF-β1 signaling/HIF-1α/Snail were two signaling pathways.
conclusionThese findings demonstrated that TGF-β1 signaling pathway was a significant factor of NE-induced cancer cells EMT. The data also suggested that psychological stress might be a risk factor which enhances the ability of migration or invasion of cancer cells.
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