ArticleScientific reports2026
4-Nonylphenol regulates cell proliferation and apoptosis in cervical carcinoma through the MEG3/PI3K/AKT signaling pathway.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- HPV52 predominates in cervical infections and precancerous lesions in Chongqing, China: a 6-year study linking genotypes to vaginal microecology.Frontiers in public health · 2026Article
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7 authors.
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Abstract
Long non-coding RNAs (lncRNAs) are critical regulators of carcinogenesis; however, their interaction with environmental endocrine disruptors (EEDs) in cervical cancer remains underexplored. This study aimed to investigate the role of lncRNA MEG3 in cervical carcinogenesis and its interaction with 4-Nonylphenol (4-NP), a widespread environmental contaminant. We quantified MEG3 expression using RT-qPCR in clinical specimens and cell lines, and measured urinary 4-NP levels via HPLC-MS/MS. Results showed significant MEG3 downregulation in cervical cancer tissues and elevated 4-NP levels in patients relative to healthy controls (22.37 ± 16.32 vs. 3.84 ± 2.52 ng/mL, P < 0.05). In vitro experiments indicated that 4-NP promoted HeLa cell proliferation (P < 0.05 at 72 h) while suppressing MEG3 expression in dose- and time-dependent manners. Functional restoration of MEG3 via lentiviral overexpression significantly inhibited tumor cell proliferation, migration, invasion, and induced apoptosis (P < 0.05). In vivo xenograft experiments confirmed that MEG3 overexpression suppressed tumor growth (0.03 ± 0.01 g vs. 0.56 ± 0.20 g in controls) by modulating the PI3K-Akt signaling pathway, as indicated by reduced expression of p-AKT, mTOR, PI3K, and BCL-2. Mechanistically, MEG3 overexpression counteracted the oncogenic effects of 4-NP, suggesting MEG3 as a critical mediator of 4-NP-induced carcinogenesis. These findings suggest that MEG3 may counteract 4-NP-induced oncogenic effects, highlighting its potential role as a putative mediator and candidate therapeutic target in environmental chemical-associated cervical carcinogenesis.
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