The repressor Capicua is a barrier to lung tumor development driven by Kras/Trp53 mutations.

doi:10.1038/s44321-025-00326-z

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Community

Back to search

Article

The repressor Capicua is a barrier to lung tumor development driven by Kras/Trp53 mutations.

EMBO molecular medicine - 1 Dec 2025

Ballesteros-González Irene, Hernández-Navas Iván, Brehey Oksana, Lechuga Carmen G, Salmón Marina, Scotece Morena, Velasco-Vicente Ricardo, Flores-Gómez Alejandra A, Cebriá Antonio, Simón-Carrasco Lucía, Jiménez Gerardo, Musteanu Monica, Guerra Carmen, Domínguez Orlando, Caleiras Eduardo, Blanco-Aparicio Carmen, Pons Tirso, Ferrer Irene, Paz-Ares Luis, Torres-Ruiz Raul, Rodríguez-Perales Sandra, Barbacid Mariano, Drosten Matthias

Abstract excerpt

KRAS mutations are responsible for a quarter of all lung adenocarcinomas. However, the molecular mechanisms linking these mutations and their frequent secondary dosage amplification to tumor formation are still not fully understood. While ample evidence supports a crucial role for the MAPK pathway in tumor development, the primary effectors targeted by this pathway remain largely unexplored. Here we identify the...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Adenocarcinoma of Lung

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Drug Resistance, Neoplasm

Share to Gene Knockdown Techniques

Share to MAP Kinase Signaling System

Share to Neoplasms, Experimental

Share to Protein Kinase Inhibitors

Share to Proto-Oncogene Proteins p21(ras)

Share to Repressor Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 41219537
DOI: 10.1038/s44321-025-00326-z
PMCID: PMC12686060

Genes

CIC
KRAS

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The repressor Capicua is a barrier to lung tumor development driven by Kras/Trp53 mutations.PMID 41219537Read ↗

The Capicua tumor suppressor: a gatekeeper of Ras signaling in development and cancerSemantic proximity Read ↗

CRACD suppresses neuroendocrinal plasticity of lung adenocarcinomaSemantic proximity Read ↗

Comparative transcriptome analysis of isogenic cell line models and primary cancers links capicua ( CIC ) loss to activation of the MAPK signalling cascadeSemantic proximity Read ↗

Inactivation of Capicua in adult mice causes T-cell lymphoblastic lymphoma.Semantic proximity Read ↗

p53 governs an AT1 differentiation programme in lung cancer suppression.Semantic proximity Read ↗

Loss of Capicua alters early T cell development and predisposes mice to T cell lymphoblastic leukemia/lymphoma.Semantic proximity Read ↗

Early-stage lung adenocarcinoma is driven by an injury-associated, plastic cell state dependent on a KRAS-ITGA3-SRC axisSemantic proximity Read ↗

Epigenetic basis of oncogenic-Kras-mediated epithelial-cellular proliferation and plasticity.Semantic proximity Read ↗

Definitive evidence for Club cells as progenitors for mutant Kras/Trp53-deficient lung cancer.Semantic proximity Read ↗

A new mode of DNA binding distinguishes Capicua from other HMG-box factors and explains its mutation patterns in cancer.Semantic proximity Read ↗

Cic Loss Promotes Gliomagenesis via Aberrant Neural Stem Cell Proliferation and Differentiation.Semantic proximity Read ↗

AP4 suppresses DNA damage, chromosomal instability and senescence via inducing MDC1/Mediator of DNA damage Checkpoint 1 and repressing MIR22HG/miR-22-3pSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.