ArticleMolecular cancer research : MCR2015
Transposon Mutagenesis Screen Identifies Potential Lung Cancer Drivers and CUL3 as a Tumor Suppressor.
Article in Molecular cancer research : MCR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- Cullin-3 adaptor SHKBP1 inhibits SQSTM1/p62 oligomerization and Keap1 sequestration.The Journal of cell biology · 2026Article
- Case Report: Ivonescimab in EGFR-mutant lung cancer with baseline malignant pleural effusion and acquired complex resistance.Frontiers in immunology · 2025Article
- Knockdown of cullin 3 inhibits progressive phenotypes and increases chemosensitivity in cholangiocarcinoma cells.Molecular medicine reports · 2024Article
- The Ubiquitin-Proteasome System in Tumor Metabolism.Cancers · 2023Review
- Significance of a PTEN Mutational Status-Associated Gene Signature in the Progression and Prognosis of Endometrial Carcinoma.Oxidative medicine and cellular longevity · 2022Article
- Promoterless Transposon Mutagenesis Drives Solid Cancers via Tumor Suppressor Inactivation.Cancers · 2021Article
- Cullin3 deficiency shapes tumor microenvironment and promotes cholangiocarcinoma in liver-specific Smad4/Pten mutant mice.International journal of biological sciences · 2021Article
- In vivo functional screening for systems-level integrative cancer genomics.Nature reviews. Cancer · 2020Review
- The role of natural products in revealing NRF2 function.Natural product reports · 2020Review
- Transposon Insertion Mutagenesis in Mice for Modeling Human Cancers: Critical Insights Gained and New Opportunities.International journal of molecular sciences · 2020Review
- Functional Genomic Screening Independently Identifies CUL3 as a Mediator of Vemurafenib Resistance via Src-Rac1 Signaling Axis.Frontiers in oncology · 2020Article
- Analysis on GENIE reveals novel recurrent variants that affect molecular diagnosis of sizable number of cancer patients.BMC cancer · 2019Article
- Sleeping Beauty Mouse Models of Cancer: Microenvironmental Influences on Cancer Genetics.Frontiers in oncology · 2019Review
- The number of titrated microRNA species dictates ceRNA regulation.Nucleic acids research · 2018Article
- Advances in functional genetic screening with transposons and CRISPR/Cas9 to illuminate cancer biology.Current opinion in genetics & development · 2018Review
- Increased Expression of Cullin 3 in Nasopharyngeal Carcinoma and Knockdown Inhibits Proliferation and Invasion.Oncology research · 2018Article
- Gene Profiling in Patients with Systemic Sclerosis Reveals the Presence of Oncogenic Gene Signatures.Frontiers in immunology · 2018Article
- Variants in the 3'-untranslated region of CUL3 is associated with risk of esophageal squamous cell carcinoma.Journal of Cancer · 2018Article
- CRISPR/Cas9 Genetic Modification ofDrug metabolism and disposition: the biological fate of chemicals · 2017Article
- Genomic analysis of oesophageal squamous-cell carcinoma identifies alcohol drinking-related mutation signature and genomic alterations.Nature communications · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
unlabelledNon-small cell lung cancers (NSCLC) harbor thousands of passenger events that hide genetic drivers. Even highly recurrent events in NSCLC, such as mutations in PTEN, EGFR, KRAS, and ALK, are detected, at most, in only 30% of patients. Thus, many unidentified low-penetrant events are causing a significant portion of lung cancers. To detect low-penetrance drivers of NSCLC, a forward genetic screen was performed in mice using the Sleeping Beauty (SB) DNA transposon as a random mutagen to generate lung tumors in a Pten-deficient background. SB mutations coupled with Pten deficiency were sufficient to produce lung tumors in 29% of mice. Pten deficiency alone, without SB mutations, resulted in lung tumors in 11% of mice, whereas the rate in control mice was approximately 3%. In addition, thyroid cancer and other carcinomas, as well as the presence of bronchiolar and alveolar epithelialization, in mice deficient for Pten were also identified. Analysis of common transposon insertion sites identified 76 candidate cancer driver genes. These genes are frequently dysregulated in human lung cancers and implicate several signaling pathways. Cullin3 (Cul3), a member of a ubiquitin ligase complex that plays a role in the oxidative stress response pathway, was identified in the screen and evidence demonstrates that Cul3 functions as a tumor suppressor. IMPLICATIONS: This study identifies many novel candidate genetic drivers of lung cancer and demonstrates that CUL3 acts as a tumor suppressor by regulating oxidative stress.
Indexed as
Identifiers
What OpenQuestion holds
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.