ArticleFrontiers in cell and developmental biology2020
Fra-1 Inhibits Cell Growth and the Warburg Effect in Cervical Cancer Cells via STAT1 Regulation of the p53 Signaling Pathway.
Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- The Role of FOSL1 in Inflammatory Bowel Disease (IBD) Pathogenesis and IBD-Associated Tumorigenesis.Biomolecules · 2026Review
- Stratified and Quantified Score Construction of Low-Grade Glioma Samples Based on TP53 Signaling Pathway.BioMed research international · 2026Article
- Review
- Fra-1 promotes gastric cancer progression by regulating macrophage polarization and transcriptionally activating HMGA2 expression.Cell death discovery · 2025Article
- Single-Cell Transcriptomics Unveils the Mechanistic Role of FOSL1 in Cutaneous Wound Healing.Biomedicines · 2025Article
- Roles of human papillomavirus in cancers: oncogenic mechanisms and clinical use.Signal transduction and targeted therapy · 2025Review
- Uncoupling protein 2 and signal transducer and activator of transcription 1 are targets of human papillomavirus oncoproteins and may be prognostic markers for cervical cancer development.Frontiers in oncology · 2025Article
- FRA1 (Frontiers in cell and developmental biology · 2025Article
- SenMayo transcriptomic senescence panel highlights glial cells in the ageing mouse and human retina.npj aging · 2024Article
- The role of circular RNA targeting IGF2BPs in cancer-a potential target for cancer therapy.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Article
- FOSL1's Oncogene Roles in Glioma/Glioma Stem Cells and Tumorigenesis: A Comprehensive Review.International journal of molecular sciences · 2024Review
- Mitochondrial protein isoleucyl-tRNA synthetase 2 in tumor cells as a potential therapeutic target for cervical cancer.CytoJournal · 2024Article
- Glucose metabolism reprogramming in gynecologic malignant tumors.Journal of Cancer · 2024Review
- NR1H4-mediated circRHOBTB3 modulates the proliferation, metastasis, and Warburg effects of cervical cancer through interacting with IGF2BP3.Molecular and cellular biochemistry · 2023Article
- Overexpression of FRA1 (Cells · 2023Article
- FOS-Like Antigen 1 Expression Was Associated With Survival of Hepatocellular Carcinoma Patients.World journal of oncology · 2023Article
- Candidate Genes and Pathways in Cervical Cancer: A Systematic Review and Integrated Bioinformatic Analysis.Cancers · 2023Review
- Fra-1 induces apoptosis and neuroinflammation by targeting S100A8 to modulate TLR4 pathways in spinal cord ischemia/reperfusion injury.Brain pathology (Zurich, Switzerland) · 2023Article
- Decision tree algorithm predicts hepatocellular carcinoma among chronic hepatitis C patients following viral eradication.American journal of cancer research · 2023Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The oncogenesis of cervical cancer is a multi-factor and multi-step process, and major risk factors include oncogene activation with tumor suppressor gene inactivation, viral factors, and immune factors. For example, the human papillomavirus (HPV) has been linked to the occurrence of cervical cancer. At present, the pathogenesis of cervical cancer remains unclear. Fra-1 (Fos-related antigen 1, also known as FOSL1) is a member of the Fos family and an important nuclear transcription factor that regulates normal cell growth, differentiation, and apoptosis. In the present study, we found that Fra-1 inhibited the proliferation of cervical cancer cells while also promoting apoptosis and affecting cell cycle distribution. Moreover, Fra-1 up-regulated STAT1 expression and modulated p53 signal pathway activity in cervical cancer cells. Overexpression of Fra-1 inhibited cell senescence by altering sirtuin 1 (SIRT1) expression in HeLa cells, and Fra-1 overexpression restored mitochondrial disorder and suppressed metabolic reprogramming in HeLa cells. Silencing of STAT1 impaired the inhibitory effect of Fra-1 on cervical cancer cell growth, while knock-down of STAT1 reversed the effect on cell senescence and mitochondrial dysfunction caused by Fra-1 in HeLa cells. Silencing of STAT1 also recovered metabolic reprogramming in cervical cancer cells. In summary, our results show that Fra-1 inhibited cervical cancer cell growth and the Warburg effect via STAT1-mediated regulation of the p53 signaling pathway.
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