ArticleCancer cell international2019
Long non-coding RNA MEG3 inhibits cervical cancer cell growth by promoting degradation of P-STAT3 protein via ubiquitination.
Article in Cancer cell international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 63 citations in OpenAlex.
- Long noncoding RNAs in female malignancies: critical review of molecular mechanisms, clinical gaps, and therapeutic perspectives.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Review
- Integrating Biomarkers into Cervical Cancer Screening-Advances in Diagnosis and Risk Prediction: A Narrative Review.Diagnostics (Basel, Switzerland) · 2025Review
- Unraveling the mechanisms of LncRNAs in cervical cancer: a comprehensive review.Cell death discovery · 2025Review
- Drug Repositioning for HPV Clade-Specific Cervicouterine Cancer Using the OCTAD Pipeline.International journal of molecular sciences · 2025Article
- LncRNA MEG3/CTCF-CXCR4 axis functions in the regulation of breast cancer cell migration.Non-coding RNA research · 2025Article
- Functional characterization of dysregulated LncRNAs in BRCA and CESC highlights their role in cancer prognosis.Scientific reports · 2025Article
- Long non-coding RNA involved in the carcinogenesis of human female cancer - a comprehensive review.Discover oncology · 2025Review
- Deciphering the mysteries of MEG3 LncRNA and its implications in genitourinary cancers.Frontiers in oncology · 2025Review
- LncRNA MEG3 Inhibits the Epithelial-mesenchymal Transition of Bladder Cancer Cells through the Snail/E-cadherin Axis.Current medical science · 2024Article
- mJournal of translational medicine · 2024Article
- Malat1 regulates PMN-MDSC expansion and immunosuppression through p-STAT3 ubiquitination in sepsis.International journal of biological sciences · 2024Article
- The role of long non-coding RNAs and circular RNAs in cervical cancer: modulating miRNA function.Frontiers in cell and developmental biology · 2024Review
- Nanoconjugated long non-coding RNA MEG3 as a new therapeutic approach for Hepatocellular carcinoma.Heliyon · 2023Article
- Sildenafil Inhibits the Growth and Epithelial-to-mesenchymal Transition of Cervical Cancer via the TGF-β1/Smad2/3 Pathway.Current cancer drug targets · 2023Article
- The Biological Roles and Molecular Mechanisms of Long Non-Coding RNA MEG3 in the Hallmarks of Cancer.Cancers · 2022Review
- Review
- Ectopic expression of lncRNA MVIH as a potential diagnostic biomarker in cervical cancer.Genes & cancer · 2022Article
- Molecular Mechanisms of HIV Protease Inhibitors Against HPV-Associated Cervical Cancer: Restoration ofFrontiers in molecular biosciences · 2022Review
- A review of current evidence about lncRNA MEG3: A tumor suppressor in multiple cancers.Frontiers in cell and developmental biology · 2022Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMaternally expressed 3 (MEG3) plays an important role in cervical cancer development, but its exact role remains unclear. Here, we explored the specific regulatory mechanism of MEG3 and its downstream proteins in cervical cancer cells.
methodsThe effect of MEG3 on tumor formation ability of cervical cancer cells was determined in nude mice. The direct binding of MEG3 to phosphorylated signal transducer and activator of transcription 3 (P-STAT3) was detected by RNA pull-down and RNA-binding protein immunoprecipitation (RIP) assays. Cycloheximide (CHX)-chase and ubiquitination assays were performed to determine the regulatory effect of MEG3 on P-STAT3 ubiquitination. Clone formation assay and flow cytometry were used to evaluate the effect of the MEG3-STAT3 regulatory axis on cell proliferation and apoptosis.
resultsIn vivo tumor formation experiments showed that MEG3 inhibited the tumor formation ability of cervical cancer cells. RNA pull-down and RIP assays demonstrated that MEG3 bound directly to P-STAT3 protein. CHX-chase and ubiquitination assay results showed that MEG3 promoted P-STAT3 degradation via ubiquitination. Clone formation assay and flow cytometry analysis results revealed that the inhibitory effect of MEG3 on P-STAT3 promoted apoptosis and inhibited proliferation of cervical cancer cells.
conclusionMEG3 binds to P-STAT3 in cervical cancer cells, resulting in P-STAT3 ubiquitination and degradation and apoptosis and inhibition of proliferation of tumor cells. The in-depth elaboration of the MEG3-STAT3 regulatory axis in cervical cancer may clarify the mechanism of action of MEG3 and provide new ideas for cervical cancer treatment.
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