ArticleCancer gene therapy2022
LncRNA MAFG-AS1 promotes the malignant phenotype of ovarian cancer by upregulating NFKB1-dependent IGF1.
Article in Cancer gene therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.
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Who cites it
17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 28 citations in OpenAlex.
- NFKB1 as a key player in Tumor biology: from mechanisms to therapeutic implications.Cell biology and toxicology · 2025Pooled it
- Correlation between long non-coding RNA MAFG-AS1 and cancer prognosis: a meta-analysis.Frontiers in oncology · 2023Pooled it
- Review
- Pathogenic role and therapeutic targets of nuclear factor-κB signaling pathway in cancer (Review).Oncology letters · 2025Review
- Molecular pathology of microRNA-339 during tumor progression.Cell division · 2025Review
- Overexpression of MAFG-AS1 in ovarian cancer promotes glucose metabolism reprogramming and malignant biological behavior of ovarian cancer cells by regulating HIF-1α.Discover oncology · 2025Article
- Article
- The Role of Long Non-Coding RNAs in Ovarian Cancer Cells.International journal of molecular sciences · 2024Review
- Article
- DNA Methylation of a Group of Long Non-Coding RNA Genes at Different Stages of Ovarian Cancer Dissemination.Bulletin of experimental biology and medicine · 2024Article
- Carcinogenic roles of MAFG-AS1 in human cancers.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024Review
- LncRNA MAFG-AS1 is involved in human cancer progression.European journal of medical research · 2023Review
- The Role of EMT-Related lncRNAs in Ovarian Cancer.International journal of molecular sciences · 2023Review
- Single-cell and bulk RNA sequencing reveal ligands and receptors associated with worse overall survival in serous ovarian cancer.Cell communication and signaling : CCS · 2022Article
- CircESRP1 enhances metastasis and epithelial-mesenchymal transition in endometrial cancer via the miR-874-3p/CPEB4 axis.Journal of translational medicine · 2022Article
- Long Non-Coding RNA MAFG-AS1 as a Potential Biomarker for Hepatocellular Carcinoma: Linkage with Tumor Features, Markers, Liver Functions, and Survival Profile.Frontiers in surgery · 2022Article
- 5-Methylcytosine RNA Methyltransferases-Related Long Non-coding RNA to Develop and Validate Biochemical Recurrence Signature in Prostate Cancer.Frontiers in molecular biosciences · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNAs (lncRNAs) were recently recognized to vitally function in a variety of cancer cellular events, including epithelial-mesenchymal transition (EMT), invasion, and migration, particularly in ovarian cancer (OC). Herein, we sought to investigate the potential role of MAFG-AS1 in the malignant behaviors of OC cells. The binding affinity between MAFG-AS1, miR-339-5p, NFKB1 or IGF1 was characterized so as to identify the underlying mechanism of corresponding their interactions. We conducted MAFG-AS1 overexpression or knockdown along with NFKB1 and IGF1 silencing to examine their effects on the EMT, migration, and invasion of OC cells. Tumors were xenografted in nude mice to validate the in vitro findings. Our data showed significantly high expression pattern of MAFG-AS1 in the OC tissues and cells. Further mechanistic investigations revealed that MAFG-AS1 upregulated the IGF1 expression pattern through recruitment of NFKB1, whereas MAFG-AS1 upregulated the NFKB1 expression pattern through binding to miR-339-5p. Thus, MAFG-AS1 overexpression accelerated the EMT, invasion, and migration of OC cells, which could be annulled by silencing of IGF1 or NFKB1. Besides, our in vitro findings were successfully recapitulated in the xenograft mice. These results determined that MAFG-AS1 stimulated the OC malignant progression by upregulating the NFKB1-mediated IGF1 via miR-339-5p, thus highlighting a novel potential therapeutic target against OC.
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