ArticlePLoS genetics2014
A mouse model uncovers LKB1 as an UVB-induced DNA damage sensor mediating CDKN1A (p21WAF1/CIP1) degradation.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 39 citations in OpenAlex.
- Molecular insights and therapeutic implications for the tumor suppressor role of LKB1 in non-small cell lung cancer.Cancer letters · 2026Review
- Myeloid infiltration and epidermal dysregulation characterize cutaneous photosensitivity in systemic lupus erythematosus.Science translational medicine · 2026Article
- Review
- Transcriptional reprogramming triggered by neonatal UV radiation or Lkb1 loss prevents BRAFOncogene · 2025Article
- Loss of Lkb1 cooperates with BrafMolecular oncology · 2025Article
- Breast cancer genomic analyses reveal genes, mutations, and signaling networks.Functional & integrative genomics · 2024Article
- STK11 loss leads to YAP1-mediated transcriptional activation in human KRAS-driven lung adenocarcinoma cell lines.Cancer gene therapy · 2024Article
- CDKN1A/p21 in Breast Cancer: Part of the Problem, or Part of the Solution?International journal of molecular sciences · 2023Review
- Federated Learning for Sparse Bayesian Models with Applications to Electronic Health Records and Genomics.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2023Article
- Revisiting the Function of p21International journal of molecular sciences · 2022Review
- Genetic Connections and Convergent Evolution of Tropical Indigenous Peoples in Asia.Molecular biology and evolution · 2022Article
- The Tumor Suppressor Kinase LKB1: Metabolic Nexus.Frontiers in cell and developmental biology · 2022Review
- Evolutionary selection identifies critical immune-relevant genes in lung cancer subtypes.Frontiers in genetics · 2022Article
- Implications of Oxidative Stress in the Pathogenesis and Treatment of Hyperpigmentation Disorders.Oxidative medicine and cellular longevity · 2022Review
- Peutz-Jeghers syndrome: Skin manifestations and endocrine anomalies (Review).Experimental and therapeutic medicine · 2021Review
- AMPKα-like proteins as LKB1 downstream targets in cell physiology and cancer.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Inhibition of β-Catenin Activity Abolishes LKB1 Loss-Driven Pancreatic Cystadenoma in Mice.International journal of molecular sciences · 2021Article
- Skin Pigmentation Abnormalities and Their Possible Relationship with Skin Aging.International journal of molecular sciences · 2021Review
- Article
- Emerging Therapeutic Implications of STK11 Mutation: Case Series.The oncologist · 2020Article
Corrections and comments
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Authors and funding
17 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exposure to ultraviolet (UV) radiation from sunlight accounts for 90% of the symptoms of premature skin aging and skin cancer. The tumor suppressor serine-threonine kinase LKB1 is mutated in Peutz-Jeghers syndrome and in a spectrum of epithelial cancers whose etiology suggests a cooperation with environmental insults. Here we analyzed the role of LKB1 in a UV-dependent mouse skin cancer model and show that LKB1 haploinsufficiency is enough to impede UVB-induced DNA damage repair, contributing to tumor development driven by aberrant growth factor signaling. We demonstrate that LKB1 and its downstream kinase NUAK1 bind to CDKN1A. In response to UVB irradiation, LKB1 together with NUAK1 phosphorylates CDKN1A regulating the DNA damage response. Upon UVB treatment, LKB1 or NUAK1 deficiency results in CDKN1A accumulation, impaired DNA repair and resistance to apoptosis. Importantly, analysis of human tumor samples suggests that LKB1 mutational status could be a prognostic risk factor for UV-induced skin cancer. Altogether, our results identify LKB1 as a DNA damage sensor protein regulating skin UV-induced DNA damage response.
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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.