ArticleRNA biology2021
IGF2BP1 is a targetable SRC/MAPK-dependent driver of invasive growth in ovarian cancer.
Article in RNA biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Systematic analysis of IGF2BP family members in non-small-cell lung cancer.Human genomics · 2024Pooled it
- Sex determines the natural killer cell-mediated immunity against pancreatic cancer.Oncoimmunology · 2026Article
- Master Regulator SMC1A, Stabilized by N6-Methyladenosine Reader IGF2BP1, Promotes HCC Progression Through Facilitating Enhancer-Promoter Interaction of Nestin.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Inhibition of RNA-binding proteins enhances immunotherapy in ovarian cancer.Signal transduction and targeted therapy · 2025Article
- Selectively Inhibition of MAPK pathway showed positive effects on Porcine embryo-derived stem cells pluripotency.Scientific reports · 2025Article
- AVJ16 inhibits lung carcinoma by targeting IGF2BP1.Oncogene · 2025Article
- IGF2BP1 promotes the progression of head and neck squamous cell carcinoma by activating PI3K/AKT/mTOR signaling pathway and inducing epithelial-mesenchymal transition.World journal of surgical oncology · 2025Article
- IGF2BP2 binding to CPSF6 facilitates m6A-mediated alternative polyadenylation of PUM2 and promotes malignant progression in ovarian cancer.Clinical and translational medicine · 2025Article
- The IGF2BP1 oncogene is a druggable mNAR cancer · 2025Article
- Epigenetic regulation in oogenesis and fetal development: insights into m6A modifications.Frontiers in immunology · 2025Review
- Ferroptosis contributes to the progression of female-specific neoplasms, from breast cancer to gynecological malignancies in a manner regulated by non-coding RNAs: Mechanistic implications.Non-coding RNA research · 2024Review
- Insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) in hematological diseases.Molecular medicine (Cambridge, Mass.) · 2024Review
- RAVER1 hinders lethal EMT and modulates miR/RISC activity by the control of alternative splicing.Nucleic acids research · 2024Article
- Emerging role of m6A modification in ovarian cancer: progression, drug resistance, and therapeutic prospects.Frontiers in oncology · 2024Review
- Elevated expression of the RNA-binding protein IGF2BP1 enhances the mRNA stability of INHBA to promote the invasion and migration of esophageal squamous cancer cells.Experimental hematology & oncology · 2023Article
- Role of the RNA-binding protein family in gynecologic cancers.American journal of cancer research · 2023Review
- SP1-induced lncRNA MCF2L-AS1 promotes cisplatin resistance in ovarian cancer by regulating IGF2BP1/IGF2/MEK/ERK axis.Journal of gynecologic oncology · 2022Article
- Ovarian cancer subtypes based on the regulatory genes of RNA modifications: Novel prediction model of prognosis.Frontiers in endocrinology · 2022Article
- La protein regulates protein expression by binding with the mRNAs of target genes and participates the pathological process of ovarian cancer.Frontiers in oncology · 2022Article
- Novel insights into mInternational journal of biological sciences · 2022Review
Corrections and comments
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Authors and funding
17 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial-to-mesenchymal transition (EMT) is a hallmark of aggressive, mesenchymal-like high-grade serous ovarian carcinoma (HGSOC). The SRC kinase is a key driver of cancer-associated EMT promoting adherens junction (AJ) disassembly by phosphorylation-driven internalization and degradation of AJ proteins. Here, we show that the IGF2 mRNA-binding protein 1 (IGF2BP1) is up-regulated in mesenchymal-like HGSOC and promotes SRC activation by a previously unknown protein-ligand-induced, but RNA-independent mechanism. IGF2BP1-driven invasive growth of ovarian cancer cells essentially relies on the SRC-dependent disassembly of AJs. Concomitantly, IGF2BP1 enhances ERK2 expression in an RNA-binding dependent manner. Together this reveals a post-transcriptional mechanism of interconnected stimulation of SRC/ERK signalling in ovarian cancer cells. The IGF2BP1-SRC/ERK2 axis is targetable by the SRC-inhibitor saracatinib and MEK-inhibitor selumetinib. However, due to IGF2BP1-directed stimulation, only combinatorial treatment effectively overcomes the IGF2BP1-promoted invasive growth in 3D culture conditions as well as intraperitoneal mouse models. In conclusion, we reveal an unexpected role of IGF2BP1 in enhancing SRC/MAPK-driven invasive growth of ovarian cancer cells. This provides a rationale for the therapeutic benefit of combinatorial SRC/MEK inhibition in mesenchymal-like HGSOC.
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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.