ArticleOncogene2000
The RAS oncogene induces genomic instability in thyroid PCCL3 cells via the MAPK pathway.
Article in Oncogene, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.
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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.
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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
71 citing papers in PubMed, 1 synthesis or guideline pooled it, 189 citations in OpenAlex.
- Management Guidelines for Children with Thyroid Nodules and Differentiated Thyroid Cancer.Thyroid : official journal of the American Thyroid Association · 2015Guideline
- Single-cell transcriptomic analysis identifies decreasedTranslational cancer research · 2026Article
- Immunophenotypic Panel for Comprehensive Characterization of Aggressive Thyroid Carcinomas.Cells · 2025Article
- High risk factors, molecular features and clinical management for radioactive iodine-refractory differentiated thyroid carcinoma.Frontiers in oncology · 2025Review
- Mouse Models to Examine Differentiated Thyroid Cancer Pathogenesis: Recent Updates.International journal of molecular sciences · 2023Review
- DNA replication stress and mitotic catastrophe mediate sotorasib addiction in KRASJournal of biomedical science · 2023Article
- Using CRISPR/Cas9 to Edit a Thyroid Cancer Cell Line.Advances in experimental medicine and biology · 2023Article
- Topoisomerase 1-dependent R-loop deficiency drives accelerated replication and genomic instability.Cell reports · 2022Article
- Molecular features of aggressive thyroid cancer.Frontiers in oncology · 2022Review
- Promoter Methylation of Tumor Suppressors in Thyroid Carcinoma: A Systematic Review.Iranian journal of public health · 2021Review
- Review
- Significance of RAS Mutations in Thyroid Benign Nodules and Non-Medullary Thyroid Cancer.Cancers · 2021Review
- Evidence of Cooperation between Hippo Pathway andCancers · 2021Article
- α-Enolase Lies Downstream of mTOR/HIF1α and Promotes Thyroid Carcinoma Progression by Regulating CST1.Frontiers in cell and developmental biology · 2021Article
- FAM172A promotes follicular thyroid carcinogenesis and may be a marker of FTC.Endocrine-related cancer · 2020Article
- RAS Subcellular Localization Inversely Regulates Thyroid Tumor Growth and Dissemination.Cancers · 2020Article
- Association of Rs61764370 polymorphism within let-7 microRNA-binding site with lung cancer in Iranian population.African health sciences · 2020Article
- Molecular testing in the diagnosis of differentiated thyroid carcinomas.Gland surgery · 2018Review
- Centrosome aberrations and chromosome instability contribute to tumorigenesis and intra-tumor heterogeneity.Journal of cancer metastasis and treatment · 2018Article
- The E2F activators control multiple mitotic regulators and maintain genomic integrity through Sgo1 and BubR1.Oncotarget · 2017Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Activating mutations of RAS are thought to be early events in the evolution of thyroid follicular neoplasms. We used a doxycycline-inducible expression system to explore the acute effects of H-RAS12 on genomic stability in thyroid PCCL3 cells. At 2-3 days (first or second cell cycle) there was a significant increase in the frequency of micronucleation. Treatment of cells with YVAD-CHO inhibited RAS-induced apoptosis, but had no effect on micronucleation. The effects of H-RAS(V12) were mediated by activation of MAPK, as treatment with PD98059 at concentrations verified to selectively inhibit MEK1 reduced the frequency of prevalence of cells with micronuclei. In addition, doxycycline-inducible expression of a constitutively active MEK1, but not of a mutant RAC1, mimicked the effects of H-RAS(V12). The effects of H-RAS(V12) on genome destabilization were apparent even though the sequence of p53 in PCCL3 cells was confirmed to be wild-type. Acute activation of H-RAS(V12) evoked a proportional increase in both CREST negative and CREST positive micronuclei, indicating that both clastogenic and aneugenic effects were involved. H-RAS(V12) and activated MEK1 also induced centrosome amplification, and chromosome misalignment. Evidence that acute expression of constitutively activated RAS destabilizes the genome of PCCL3 cells is consistent with a mode of tumor initiation in which this oncogene promotes phenotypic progression by predisposing to large scale genomic abnormalities.
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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.