ArticleGenes & genomics2025
Propylparaben-induced endoplasmic reticulum stress triggers G2/M phase cell cycle arrest and initiates caspase-3-dependent apoptosis in human lung cells.
Article in Genes & genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
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Who cites it
4 citing papers in PubMed.
- Parametric hypothesis testing for pathway based hierarchical structural component models.Genes & genomics · 2026Article
- Exposure to Urinary and Dust Parabens: Compound-Specific Risks for Pediatric Respiratory Allergic Phenotypes.Toxics · 2026Article
- Article
- Genotoxic and Toxicopathological Responses to Ethylparaben in Plants: Potential Impacts to Crop Yields.Toxics · 2025Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
backgroundPropylparaben (PrP) is commonly used as an antimicrobial agent in food, cosmetics, and pharmaceuticals. While recent studies have shown that PrP exposure can cause various disruptions in cellular physiology, the precise mechanisms behind these effects remain unclear.
objectiveIn this study, we sought to examine the cytotoxic effects of PrP exposure on human lung cells in a dose- and time-dependent manner. We utilized flow cytometry to analyze the expression of proteins associated with the cell cycle and apoptosis at the single-cell level.
resultsOur results showed that PrP treatment leads to a significant upregulation of genes related to ER stress. The activation of ER stress results in a decrease in cyclin B1 levels, which subsequently causes cell cycle arrest at the G2/M phase. After 48 h of PrP exposure, the unfolded protein response (UPR) triggers an apoptotic signaling pathway, increasing the number of cells undergoing caspase-3-mediated apoptosis. Together, these physiological changes lead to a reduction in cell viability in the presence of PrP.
conclusionThese findings suggest that PrP exerts harmful effects on human lung cells by activating ER stress, which can lead to apoptosis and cell cycle arrest.
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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.