ArticleOncology reports2021
Waterpipe smoke condensate influences epithelial to mesenchymal transition and interferes with the cytotoxic immune response in non-small cell lung cancer cell lines.
Article in Oncology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Waterpipe Smoke-Induced N6-Methyladenosine Modification Promotes the Progression of Oral Squamous Cell Carcinoma.International dental journal · 2026Article
- Waterpipe smoke condensate activates the oncogenes and promotes epithelial-mesenchymal transition to cause oral cancer.Odontology · 2026Article
- The CCL2-CCR2 axis in primary lung cancer and pulmonary metastasis: from molecular mechanisms to therapeutic potentials.Frontiers in immunology · 2026Review
- Waterpipe smoke condensate activates autophagy in non-tumorigenic lung epithelial cells: Implications for inflammation and stemness.PloS one · 2026Article
- Impact of prolonged exposure to occasional and regular waterpipe smoke on cardiac injury, oxidative stress and mitochondrial dysfunction in male mice.Frontiers in physiology · 2024Article
- Key challenges for in vitro testing of tobacco products for regulatory applications: Recommendations for dosimetry.Drug testing and analysis · 2023Article
- Predicting thrombotic cardiovascular outcomes induced by waterpipe-associated chemicals using comparative toxicogenomic database: Genes, phenotypes, and pathways.Life sciences · 2023Article
- Genomic Analysis of Waterpipe Smoke-Induced Lung Tumor Autophagy and Plasticity.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Waterpipe tobacco smoking (WPS) continues to spread globally and presents serious health hazards. The aim of the present study was to investigate the effects of treatment with WPS condensate (WPSC) on lung cell proliferation and plasticity as well as tumor cell recognition and killing by natural killer (NK) cells using cytotoxicity assays. The results indicated that exposure of normal and cancer lung cell lines to WPSC resulted in a decrease in their in vitro growth in a dose-dependent manner and it induced tumor senescence. In addition, WPSC selectively caused DNA damage as revealed by an increase in γH2AX and 53BP1 in tumor lung cells. To gain further insight into the molecular mechanisms altered by WPSC, we conducted a global comprehensive transcriptome analysis of WPSC-treated tumor cells. Data analysis identified an expression profile of genes that best distinguished treated and non-treated cells involving several pathways. Of these pathways, we focused on those involved in epithelial to mesenchymal transition (EMT) and stemness. Results showed that WPSC induced an increase in SNAI2 expression associated with EMT, ACTA2 and SERPINE2 were involved in invasion and CD44 was associated with stemness. Furthermore, WPSC exposure increased the expression of inflammatory response genes including CASP1, IL1B, IL6 and CCL2. While immune synapse formation between NK and WPSC-treated lung cancer target cells was not affected, the capacity of NK cells to kill these target cells was reduced. The data reported in the present study are, to the best of our knowledge, the first in vitro demonstration of WPSC effects on lung cellular parameters providing evidence of its potential involvement in tumor physiology and development.
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