ArticleOncotarget2014
Caveolin-1 regulates lung cancer stem-like cell induction and p53 inactivation in carbon nanotube-driven tumorigenesis.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- Caveolin-1: an ambiguous entity in breast cancer.Molecular cancer · 2025Review
- Identification of Candidate lncRNA and Pseudogene Biomarkers Associated with Carbon-Nanotube-Induced Malignant Transformation of Lung Cells and Prediction of Potential Preventive Drugs.International journal of environmental research and public health · 2022Article
- Investigating the Neurotoxic Impacts of Arsenic and the Neuroprotective Effects of Dictyophora Polysaccharide Using SWATH-MS-Based Proteomics.Molecules (Basel, Switzerland) · 2022Article
- Caveolin1: its roles in normal and cancer stem cells.Journal of cancer research and clinical oncology · 2021Review
- A novel TRPM7/O-GlcNAc axis mediates tumour cell motility and metastasis by stabilising c-Myc and caveolin-1 in lung carcinoma.British journal of cancer · 2020Article
- Caveolin-1 inhibits breast cancer stem cells via c-Myc-mediated metabolic reprogramming.Cell death & disease · 2020Article
- Multifaceted Roles of Caveolin-1 in Lung Cancer: A New Investigation Focused on Tumor Occurrence, Development and Therapy.Cancers · 2020Review
- The Applications of Carbon Nanotubes in the Diagnosis and Treatment of Lung Cancer: A Critical Review.International journal of nanomedicine · 2020Review
- The paracrine induction of prostate cancer progression by caveolin-1.Cell death & disease · 2019Article
- SOX9 Regulates Cancer Stem-Like Properties and Metastatic Potential of Single-Walled Carbon Nanotube-Exposed Cells.Scientific reports · 2017Article
- Induction of Slug by Chronic Exposure to Single-Walled Carbon Nanotubes Promotes Tumor Formation and Metastasis.Chemical research in toxicology · 2017Article
- Elevated expression of STIM1 is involved in lung tumorigenesis.Oncotarget · 2016Article
- Induction of cancer-associated fibroblast-like cells by carbon nanotubes dictates its tumorigenicity.Scientific reports · 2016Article
- Role of mesothelin in carbon nanotube-induced carcinogenic transformation of human bronchial epithelial cells.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Carcinogenic Potential of High Aspect Ratio Carbon Nanomaterials.Environmental science. Nano · 2016Article
- A Review on the Respiratory System Toxicity of Carbon Nanoparticles.International journal of environmental research and public health · 2016Review
- ROR1 sustains caveolae and survival signalling as a scaffold of cavin-1 and caveolin-1.Nature communications · 2016Article
- Integrated Analysis of Dysregulated ncRNA and mRNA Expression Profiles in Humans Exposed to Carbon Nanotubes.PloS one · 2016Article
- Caveolin-1, a stress-related oncotarget, in drug resistance.Oncotarget · 2015Review
- Carbon nanotubes induce apoptosis resistance of human lung epithelial cells through FLICE-inhibitory protein.Toxicological sciences : an official journal of the Society of Toxicology · 2015Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Cancer stem cells (CSCs) may represent targets for carcinogenic initiation by chemical and environmental agents. Recent studies have raised a concern over the potential carcinogenicity of carbon nanotubes (CNTs), one of the most commonly used engineered nanomaterials with asbestos-like properties. Here, we show that chronic (6-month) exposure of human lung epithelial cells to single-walled (SW) CNTs at the workplace-relevant concentration induced an emergence of lung CSCs, as indicated by the induction of CSC tumor spheres and side population (SP). These CSCs, which were found to overexpress tumor promoter caveolin-1 (Cav-1), displayed aggressive cancer phenotypes of apoptosis resistance and enhanced cell invasion and migration compared with their non-CSC counterpart. Using gene manipulation strategies, we reveal for the first time that Cav-1 plays an essential role in CSC regulation and aggressiveness of SWCNT-transformed cells partly through p53 dysregulation, consistent with their suggested role by microarray and gene ontology analysis. Cav-1 not only promoted tumorigenesis in a xenograft mouse model but also metastasis of the transformed cells to neighboring tissues. Since CSCs are crucial to the initiation and early development of carcinogenesis, our findings on CSC induction by SWCNTs and Cav-1 could aid in the early detection and risk assessment of the disease.
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Registered trials
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.