ArticleOncotarget2017
Autocrine IL-6 mediates pituitary tumor senescence.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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.
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
21 citing papers in PubMed, 34 citations in OpenAlex.
- Cellular senescence and regulated cell death in cancer: mechanisms, cross-regulatory networks and therapeutic implications.Journal of hematology & oncology · 2026Review
- Inflammatory milieu and role of epigenetic modifications in high-grade serous ovarian cancer.Clinical epigenetics · 2026Review
- Analysis of senescence in pituitary tumors from different lineages and the potential role of senolytic drugs as targeted therapies.Frontiers in endocrinology · 2026Article
- The Role of Cytokines in the Development and Functioning of the Hypothalamic-Pituitary-Gonadal Axis in Mammals in Normal and Pathological Conditions.International journal of molecular sciences · 2025Review
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- Article
- Oxidative Stress and Inflammation: Drivers of Tumorigenesis and Therapeutic Opportunities.Antioxidants (Basel, Switzerland) · 2025Review
- New insights in cellular senescence: The pituitary model.Journal of neuroendocrinology · 2025Review
- Cellular senescence in age-related cardiovascular disease: past and future.Frontiers in aging · 2025Review
- Emerging insights in senescence: pathways from preclinical models to therapeutic innovations.npj aging · 2024Review
- The SASP factor IL-6 sustains cell-autonomous senescent cells via a cGAS-STING-NFκB intracrine senescent noncanonical pathway.Aging cell · 2024Article
- Targeting inflammation as cancer therapy.Journal of hematology & oncology · 2024Review
- Role of Tumor Microenvironment in Pituitary Neuroendocrine Tumors: New Approaches in Classification, Diagnosis and Therapy.Cancers · 2023Review
- Oxidative stress in pituitary neuroendocrine tumors: Affecting the tumor microenvironment and becoming a new target for pituitary neuroendocrine tumor therapy.CNS neuroscience & therapeutics · 2023Review
- Clinical Biology of the Pituitary Adenoma.Endocrine reviews · 2022Review
- Intratumoural spatial distribution of S100B + folliculostellate cells is associated with proliferation and expression of FSH and ERα in gonadotroph tumours.Acta neuropathologica communications · 2022Article
- Architects of Pituitary Tumour Growth.Frontiers in endocrinology · 2022Review
- The two facets of gp130 signalling in liver tumorigenesis.Seminars in immunopathology · 2021Review
- Adamantinomatous craniopharyngioma as a model to understand paracrine and senescence-induced tumourigenesis.Cellular and molecular life sciences : CMLS · 2021Review
- Serum levels of IL-6, IL-8, and IL-10 are indicators of prognosis in pancreatic cancer.The Journal of international medical research · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is a stable proliferative arrest state. Pituitary adenomas are frequent and mostly benign, but the mechanism for this remains unknown. IL-6 is involved in pituitary tumor progression and is produced by the tumoral cells. In a cell autonomous fashion, IL-6 participates in oncogene-induced senescence in transduced human melanocytes. Here we prove that autocrine IL-6 participates in pituitary tumor senescence. Endogenous IL-6 inhibition in somatotroph MtT/S shRNA stable clones results in decreased SA-β-gal activity and p16INK4a but increased pRb, proliferation and invasion. Nude mice injected with IL-6 silenced clones develop tumors contrary to MtT/S wild type that do not, demonstrating that clones that escape senescence are capable of becoming tumorigenic. When endogenous IL-6 is silenced, cell cultures derived from positive SA-β-gal human tumor samples decrease the expression of the senescence marker. Our results establish that IL-6 contributes to maintain senescence by its autocrine action, providing a natural model of IL-6 mediated benign adenoma senescence.
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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.