ArticleOncotarget2014
Oncogenic RAS-induced senescence in human primary thyrocytes: molecular effectors and inflammatory secretome involved.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
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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
16 citing papers in PubMed, 21 citations in OpenAlex.
- Identification of prognostic and cellular senescence gene E2F1 of papillary thyroid carcinoma through bioinformatics analyses and experimental verification.Frontiers in genetics · 2025Article
- Review
- Senescent Thyrocytes, Similarly to Thyroid Tumor Cells, Elicit M2-like Macrophage Polarization In Vivo.Biology · 2021Article
- Chemokine-Directed Tumor Microenvironment Modulation in Cancer Immunotherapy.International journal of molecular sciences · 2021Review
- Chemokines and their Receptors: Multifaceted Roles in Cancer Progression and Potential Value as Cancer Prognostic Markers.Cancers · 2020Review
- Cancer Associated Fibroblasts and Senescent Thyroid Cells in the Invasive Front of Thyroid Carcinoma.Cancers · 2020Article
- Unmasking senescence: context-dependent effects of SASP in cancer.Nature reviews. Cancer · 2019Review
- Senescent thyrocytes and thyroid tumor cells induce M2-like macrophage polarization of human monocytes via a PGE2-dependent mechanism.Journal of experimental & clinical cancer research : CR · 2019Article
- Growth suppression by dual BRAF(V600E) and NRAS(Q61) oncogene expression is mediated by SPRY4 in melanoma.Oncogene · 2019Article
- Two-Step Senescence-Focused Cancer Therapies.Trends in cell biology · 2018Review
- Oncogene-induced senescence and its evasion in a mouse model of thyroid neoplasia.Molecular and cellular endocrinology · 2018Article
- Metformin transiently inhibits colorectal cancer cell proliferation as a result of either AMPK activation or increased ROS production.Scientific reports · 2017Article
- GSK3β activity is essential for senescence-associated heterochromatin foci (SAHF) formation induced by HMGA2 in WI38 cells.American journal of translational research · 2017Article
- Article
- Gerosuppression in confluent cells.Aging · 2014Article
- Geroconversion: irreversible step to cellular senescence.Cell cycle (Georgetown, Tex.) · 2014Review
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Oncogene-induced senescence (OIS) is a robust and sustained antiproliferative response to oncogenic stress and constitutes an efficient barrier to tumour progression. We have recently proposed that OIS may be involved in the pathogenesis of thyroid carcinoma by restraining tumour progression as well as the transition of well differentiated to more aggressive variants. Here, an OIS inducible model was established and used for dissecting the molecular mechanisms and players regulating senescence in human primary thyrocytes. We show that oncogenic RAS induces senescence in thyrocytes as judged by changes in cell morphology, activation of p16INK4a and p53/p21CIP1 tumour suppressor pathways, senescence-associated β-galactosidase (SA-β-Gal) activity, and induction of proinflammatory components including IL-8 and its receptor CXCR2. Using RNA interference (RNAi) we demonstrate that p16INK4a is necessary for the onset of senescence in primary thyrocytes as its depletion rescues RAS-induced senescence. Furthermore, we found that IL-8/CXCR2 network reinforces the growth arrest triggered by oncogenic RAS, as its abrogation is enough to resume proliferation. Importantly, we observed that CXCR2 expression coexists with OIS markers in thyroid tumour samples, suggesting that CXCR2 contributes to senescence, thus limiting thyroid tumour progression.
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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.