ArticleNature communications2019
CIC protein instability contributes to tumorigenesis in glioblastoma.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.
- Molecular Pathogenesis of Glioblastoma in Adults and Future Perspectives: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- Modeling of Capicua Family Fusion Oncoprotein-Driven Cancers Reveals Gene-Specific Functionality.Molecular cancer research : MCR · 2026Article
- ERK inhibits Capicua repressor function via multisite phosphorylation.Journal of cell science · 2026Article
- A Ubiquitination-Related Gene Prognostic Signature and the Oncogenic Role of RNF149 in Nasopharyngeal Carcinoma: scRNAseq- Based Bioinformatics and Experimental Validation.Current medicinal chemistry · 2026Article
- A multimodal knowledge-enhanced whole-slide pathology foundation model.Nature communications · 2025Article
- Molecular basis of DNA recognition by the HMG-box-C1 module of capicua.Structure (London, England : 1993) · 2025Article
- The repressor Capicua is a barrier to lung tumor development driven by Kras/Trp53 mutations.EMBO molecular medicine · 2025Article
- Molecular Biomarkers of Glioma.Biomedicines · 2025Review
- Transcriptional regulation of ETV5 by mitogen-activated protein kinase via ETS-1 in human pancreatic cancer cells.Scientific reports · 2025Article
- Transcriptional repressor Capicua is a gatekeeper of cell-intrinsic interferon responses.Cell host & microbe · 2025Article
- It's all downstream from here: RTK/Raf/MEK/ERK pathway resistance mechanisms in glioblastoma.Journal of neuro-oncology · 2025Review
- Identifying Diffuse Glioma Subtypes Based on Pathway Enrichment Evaluation.Interdisciplinary sciences, computational life sciences · 2024Article
- The genetic evolution of acral melanoma.Nature communications · 2024Article
- PJA1-mediated suppression of pyroptosis as a driver of docetaxel resistance in nasopharyngeal carcinoma.Nature communications · 2024Article
- Tumor radiogenomics in gliomas with Bayesian layered variable selection.Medical image analysis · 2023Article
- The genetic evolution of acral melanoma.bioRxiv : the preprint server for biology · 2023Article
- Article
- Capicua (CIC) mutations in gliomas in association with MAPK activation for exposing a potential therapeutic target.Medical oncology (Northwood, London, England) · 2023Article
- E26 transformation-specific transcription variant 5 in development and cancer: modification, regulation and function.Journal of biomedical science · 2023Review
- CIC reduces xCT/SLC7A11 expression and glutamate release in glioma.Acta neuropathologica communications · 2023Article
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 3 countries.
Funding
Abstract
Capicua (CIC) is a transcriptional repressor that counteracts activation of genes downstream of receptor tyrosine kinase (RTK)/Ras/ERK signaling. It is well-established that tumorigenesis, especially in glioblastoma (GBM), is attributed to hyperactive RTK/Ras/ERK signaling. While CIC is mutated in other tumors, here we show that CIC has a tumor suppressive function in GBM through an alternative mechanism. We find that CIC protein levels are negligible in GBM due to continuous proteasome-mediated degradation, which is mediated by the E3 ligase PJA1 and show that this occurs through binding of CIC to its DNA target and phosphorylation on residue S173. PJA1 knockdown increased CIC stability and extended survival using in-vivo models of GBM. Deletion of the ERK binding site resulted in stabilization of CIC and increased therapeutic efficacy of ERK inhibition in GBM models. Our results provide a rationale to target CIC degradation in Ras/ERK-driven tumors, including GBM, to increase efficacy of ERK inhibitors.
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Registered trials
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.