ArticleJournal of oral biology and craniofacial research
Nicotine mediated epithelial modulations: An
Article in Journal of oral biology and craniofacial research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 4 citations in OpenAlex.
- Short-Term Nicotine Improves Experimental Flap Survival: Implications for Different Findings in Experimental Flap Models.Medicina (Kaunas, Lithuania) · 2026Article
- Effects of smoking on palatal thickness, density, and vascularization assessed by high-frequency ultrasonography.Scientific reports · 2026Article
- Exploring the potential of selenium nanoparticles and fabricated selenium nanoparticles @vitamin C nanocomposite in mitigating nicotine-induced testicular toxicity in rats.Toxicology research · 2024Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Nicotine, the main ingredient in tobacco, acts as a key alkaloid of nearly all tobacco products and has been demonstrated to facilitate tumorigenesis and accelerate metastasis. Further traditional tobacco products have shown to give systemic oral effects such as vasoconstriction, inflammation, and delayed wound healing, however; none of the reports have confirmed the significant knowledge of oral sequel of the effect of nicotine on oral epithelial cells. So, the current study aimed to investigate the effect of nicotine on epithelial transformation to a malignant state. Material & methods: Through Result & conclusion: MTT assay demonstrated that the proliferation of epithelial cells takes place at a 150 mM concentration of nicotine. Further, we identified the significantly increased cell count and viability in nicotine-exposed cells. Further, cell cycle distribution assay results demonstrated that nicotine forced the epithelial cells to enter the first growth phase. The same influence of nicotine was observed on the PI3K/MAPK dual pathway activation assay where a greater number of nicotine exposed cells showed dual pathway activation. In conclusion, the current study determined the potential mechanism of action of nicotine on oral epithelial cell proliferation through activating the oncogenic pathway. This may help to develop novel therapeutic strategies for the prevention of malignant transformation from smokeless tobacco-caused oral cancer.
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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.