ArticleClinical and translational medicine2023
IGF2BP3 mediates the mRNA degradation of NF1 to promote triple-negative breast cancer progression via an m6A-dependent manner.
Article in Clinical and translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 25 citations in OpenAlex.
- Targeting IGF2BP3 in Cancer: From Molecular Structure and Biology to Early Drug Discovery.International journal of molecular sciences · 2026Review
- Berberine in breast cancer, a multi-targeted therapeutic agent from mechanisms to clinical translation.Molecular biology reports · 2026Review
- PLSCR1 drives chemoresistance in TNBC via METTL3/IGF2BP3-mediated mRNA stabilization and EGFR-MAPK pathway activation.Cell death & disease · 2026Article
- Combinatorial inhibition of IGF2BP3-regulated receptor tyrosine kinases offers a new therapeutic strategy for triple-negative breast cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- IGF2BP3 promotes the muscle invasion of bladder cancer via PPARγ dysregulation.Discover oncology · 2026Article
- USP10 promotes cell proliferation and gemcitabine resistance in pancreatic cancer by the regulation of IGF2BP3-STEAP3.Oncogene · 2026Article
- Mapping Non-Coding Epimutations in Breast Cancer: Advancing Epigenetics Towards Precision Medicine.Sub-cellular biochemistry · 2026Review
- TET-mediated 5hmC in breast cancer: mechanism and clinical potential.Epigenetics · 2025Review
- DNA, RNA, and histone methylation regulation enzymes and their crosstalk in colorectal carcinogenesis and progression: a review of molecular mechanisms, clinical implications, and future perspectives.Cellular & molecular biology letters · 2025Review
- Positive feedback loop of IGF2BP3/IL6ST/STAT3 facilitates malignant progression in colorectal cancer.Journal of translational medicine · 2025Article
- Integrative proteo-genomic profiling uncovers key biomarkers of lapatinib resistance in HER2-positive breast cancer.British journal of cancer · 2025Article
- The deubiquitinase USP9X and E3 ligase WWP1 orchestrate IGF2BP2 ubiquitination homeostasis to drive TNBC progression and cisplatin sensitivity.Cell death & disease · 2025Article
- A histone-centric multi-omics study shows that increased H3K4 methylation sustains triple-negative breast cancer phenotypes.Nature communications · 2025Article
- MYC/TET3-Regulated TMEM65 Activates OXPHOS-SERPINB3 Pathway to Promote Progression and Cisplatin Resistance in Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- IGF2BP3 promotes autophagy-mediated TNBC metastasis via m6A-dependent, cap-independent c-Met translation.Cell communication and signaling : CCS · 2025Article
- Ten-Eleven Translocation Family Proteins: Structure, Biological Functions, Diseases, and Targeted Therapy.MedComm · 2025Review
- RNA methylation and breast cancer: insights into m6A, m7G and m5C.Molecular biology reports · 2024Review
- Berberine inhibits the progression of breast cancer by regulating METTL3-mediated m6A modification of FGF7 mRNA.Thoracic cancer · 2024Article
- NRF2 activation by cysteine as a survival mechanism for triple-negative breast cancer cells.Oncogene · 2024Article
- LRPPRC promotes glycolysis by stabilising LDHA mRNA and its knockdown plus glutamine inhibitor induces synthetic lethality via mClinical and translational medicine · 2024Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundN6-methyladenosine (m6A) is an abundant reversible modification in eukaryotic mRNAs. Emerging evidences indicate that m6A modification plays a vital role in tumourigenesis. As a crucial reader of m6A, IGF2BP3 usually mediates the stabilisation of mRNAs via an m6A-dependent manner. But the underlying mechanism of IGF2BP3 in the tumourigenesis of triple-negative breast cancer (TNBC) is unclear.
methodsTCGA cohorts were analysed for IGF2BP3 expression and IGF2BP3 promoter methylation levels in different breast cancer subtypes. Colony formation, flow cytometry assays and subcutaneous xenograft were performed to identify the phenotype of IGF2BP3 in TNBC. RNA/RNA immunoprecipitation (RIP)/methylated RNA immunoprecipitation (MeRIP) sequencing and luciferase assays were used to certify the target of IGF2BP3 in TNBC cells.
resultsIGF2BP3 was highly expressed in TNBC cell lines and tissues. TET3-mediated IGF2BP3 promoter hypomethylation led to the upregulation of IGF2BP3. Knocking down IGF2BP3 markedly reduced the proliferation of TNBC in vitro and in vivo. Intersection co-assays revealed that IGF2BP3 decreased neurofibromin 1 (NF1) stabilisation via an m6A-dependent manner. NF1 knockdown could rescue the phenotypes of IGF2BP3 knockdown cells partially.
conclusionTET3-mediated IGF2BP3 accelerated the proliferation of TNBC by destabilising NF1 mRNA via an m6A-dependent manner. This suggests that IGF2BP3 could be a potential therapeutic target for TNBC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.