ArticleCellular & molecular biology letters2024
IGF2BP3 prevent HMGB1 mRNA decay in bladder cancer and development.
Article in Cellular & molecular biology letters, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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29 citing papers in PubMed, 24 citations in OpenAlex.
- High mobility group box 1 and its post-translational modifications: Molecular mechanisms underlying neurodegenerative disease pathogenesis.Neural regeneration research · 2026Article
- IGF2BP3 enhances paclitaxel resistance in bladder urothelial carcinoma by recognizing mMedical oncology (Northwood, London, England) · 2026Article
- Targeting IGF2BP3 in Cancer: From Molecular Structure and Biology to Early Drug Discovery.International journal of molecular sciences · 2026Review
- Prognostic and immunological implications of a mitophagy-associated gene signature in bladder cancer.Translational andrology and urology · 2026Article
- IGF2BP3 promotes epithelial ovarian cancer progression by regulating FASN expression.Scientific reports · 2026Article
- Abnormal Sialylation Promotes Chemotherapy Resistance in Bladder Cancer via the PI3K-AKT-mTOR Signaling Pathway.Cancers · 2026Article
- Comparative Evaluation of HMG Family Proteins and miR-106a-5p in Low-Grade Non-Invasive and High-Grade Muscle-Invasive Papillary Urothelial Carcinoma.International journal of molecular sciences · 2026Article
- IGF2BP3 Promoted the Overproliferation of AML Cells via Stability ofTurkish journal of haematology : official journal of Turkish Society of Haematology · 2026Article
- M6AREG 2.0: the landscape of m6A-centered crosstalk with diverse epigenetic regulation.Nucleic acids research · 2026Article
- THAP7-AS1 orchestrates IGF2BP3-mAmerican journal of cancer research · 2026Article
- Fecal microbiota transplantation: a novel strategy and challenges in the adjuvant treatment of bladder Cancer.Frontiers in microbiology · 2026Review
- HMGB1 downregulates DDX3 to activate the MAPK pathway, promoting the progression of colorectal cancer.Cancer gene therapy · 2025Article
- IGF2BP3 regulates EMP1 stability in an mCell death & disease · 2025Article
- Article
- m6A modification of non‑coding RNA: Mechanisms, functions and potential values in human diseases (Review).International journal of molecular medicine · 2025Review
- Utilizing partial information decomposition to evaluate the complex interplay between microRNA and RNA-binding protein in regulating the shared target mRNA.Scientific reports · 2025Article
- Methionine-driven YTHDF1 expression facilitates bladder cancer progression by attenuating RIG-I-modulated immune responses and enhancing the eIF5B-PD-L1 axis.Cell death and differentiation · 2025Article
- The mechanism of high mobility group box-1 in the proliferation and macrophage polarization in esophageal squamous cell carcinoma cells.European journal of medical research · 2025Article
- EZH2-Mediated PHF10 Suppression Amplifies HMGB1/NF-κB Axis That Confers Chemotherapy Resistance in Cholangiocarcinoma.Journal of cellular and molecular medicine · 2025Article
- Comment onInternational journal of biological sciences · 2025Article
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9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundIGF2BP3 functions as an RNA-binding protein (RBP) and plays a role in the posttranscriptional control of mRNA localization, stability, and translation. Its dysregulation is frequently associated with tumorigenesis across various cancer types. Nonetheless, our understanding of how the expression of the IGF2BP3 gene is regulated remains limited. The specific functions and underlying mechanisms of IGF2BP3, as well as the potential benefits of targeting it for therapeutic purposes in bladder cancer, are not yet well comprehended.
methodsThe mRNA and protein expression were examined by RT-qPCR and western blotting, respectively. The methylation level of CpG sites was detected by Bisulfite sequencing PCR (BSP). The regulation of IGF2BP3 expression by miR-320a-3p was analyzed by luciferase reporter assay. The functional role of IGF2BP3 was determined through proliferation, colony formation, wound healing, invasion assays, and xenograft mouse model. The regulation of HMGB1 by IGF2BP3 was investigated by RNA immunoprecipitation (RIP) and mRNA stability assays.
resultsWe observed a significant elevation in IGF2BP3 levels within bladder cancer samples, correlating with more advanced stages and grades, as well as an unfavorable prognosis. Subsequent investigations revealed that the upregulation of IGF2BP3 expression is triggered by copy number gain/amplification and promoter hypomethylation in various tumor types, including bladder cancer. Furthermore, miR-320a-3p was identified as another negative regulator in bladder cancer. Functionally, the upregulation of IGF2BP3 expression exacerbated bladder cancer progression, including the proliferation, migration, and invasion of bladder cancer. Conversely, IGF2BP3 silencing produced the opposite effects. Moreover, IGF2BP3 expression positively correlated with inflammation and immune infiltration in bladder cancer. Mechanistically, IGF2BP3 enhanced mRNA stability and promoted the expression of HMGB1 by binding to its mRNA, which is a factor that promotes inflammation and orchestrates tumorigenesis in many cancers. Importantly, pharmacological inhibition of HMGB1 with glycyrrhizin, a specific HMGB1 inhibitor, effectively reversed the cancer-promoting effects of IGF2BP3 overexpression in bladder cancer. Furthermore, the relationship between HMGB1 mRNA and IGF2PB3 is also observed in mammalian embryonic development, with the expression of both genes gradually decreasing as embryonic development progresses.
conclusionsOur present study sheds light on the genetic and epigenetic mechanisms governing IGF2BP3 expression, underscoring the critical involvement of the IGF2BP3-HMGB1 axis in driving bladder cancer progression. Additionally, it advocates for the investigation of inhibiting IGF2BP3-HMGB1 as a viable therapeutic approach for treating bladder cancer.
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