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<p>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, <i>P</i> &lt; 0.05). In <i>vitro</i> experiments indicated that 4-NP promoted HeLa cell proliferation (<i>P</i> &lt; 0.05 at 72&#xa0;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 (<i>P</i> &lt; 0.05). In <i>vivo</i> xenograft experiments confirmed that MEG3 overexpression suppressed tumor growth (0.03 ± 0.01&#xa0;g vs. 0.56 ± 0.20&#xa0;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.</p>

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4-Nonylphenol regulates cell proliferation and apoptosis in cervical carcinoma through the MEG3/PI3K/AKT signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月23日

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  • Wenjuan Wu,
  • Xiaoyan Ren,
  • Ying Chen,
  • Wangmei Du,
  • Geyu Liang,
  • Chuan Xu,
  • Gang Wang

摘要

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.