ArticleTobacco induced diseases2018
Effects of a natural polyphenol on nicotine-induced pancreatic cancer cell proliferation.
Article in Tobacco induced diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- Polyphenols in Pancreatic Cancer Management: Exploring the Roles and Mechanisms of Resveratrol and Epigallocatechin.Oncology research · 2025Review
- Advances in the treatment of pancreatic cancer with traditional Chinese medicine.Frontiers in pharmacology · 2023Review
- Article
- Article
- Polyphenols as Antitumor Agents Targeting Key Players in Cancer-Driving Signaling Pathways.Frontiers in pharmacology · 2021Review
- Dietary Polyphenols in Cancer Chemoprevention: Implications in Pancreatic Cancer.Antioxidants (Basel, Switzerland) · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionResveratrol (
methodsCultured AR42J cells were incubated with 100 μM nicotine for 3 min and with 100 μM resveratrol for 30 min, either alone or in combination. Proliferation assays were conducted for a period of 0 to 96 h in serum media, incubated with nicotine and resveratrol, and evaluated by MTT assay. Protein was measured in lysed cells and activation of MAPK signals was measured by western blot using purified p-ERK antibody. Co-localization of activated ERK signals was confirmed by FITC conjugated ERK antibody using immunofluorescence assay and confocal microscopy. Biomarker of lipid peroxidation was determined in cell lysates by malondialdehyde (MDA) bioassay.
resultsResveratrol significantly suppressed the nicotine-induced proliferation of acinar cells compared to untreated controls (p<0.05). Mitogen activated protein kinase (MAPK) analysis revealed up-regulation of p-ERK expression by nicotine (p<0.05) that was suppressed significantly by resveratrol (p<0.05). Co-localization of activated ERK signals was confirmed by FITC conjugated ERK antibody, and this response was reduced significantly by resveratrol. Nicotine-induced malondialdehyde formation was also suppressed by resveratrol (p<0.05).
conclusionsThe data suggest that resveratrol suppressed nicotine-induced AR42J cell proliferation. The proliferation of AR42J cells by nicotine is associated with activation of MAPK signals and induction of protein oxidation. Resveratrol suppressed lipid peroxidation and P-ERK activated signals induced by nicotine. We conclude that resveratrol acts as an effective antioxidant in reversing the nicotine induced pancreatic cancer cell proliferation.
Indexed as
Identifiers
What OpenQuestion holds
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.