ArticleThe Journal of biological chemistry2014
The nuclear receptor peroxisome proliferator-activated receptor-β/δ (PPARβ/δ) promotes oncogene-induced cellular senescence through repression of endoplasmic reticulum stress.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed, 47 citations in OpenAlex.
- Review
- Genetic and molecular mechanisms in lung cancer with interstitial pneumonia.International journal of clinical oncology · 2026Review
- Concomitant Idiopathic Pulmonary Fibrosis and Lung Cancer: An Updated Narrative Review.Advances in respiratory medicine · 2025Review
- TPL2 Promotes Gastric Cancer Progression and Chemoresistance Through a Hypoxia-Induced Positive Feedback Loop with PPARδ.International journal of biological sciences · 2025Article
- Inhibition of PERK-mediated unfolded protein response acts as a switch for reversal of residual senescence and as senolytic therapy in glioblastoma.Neuro-oncology · 2024Article
- The endoplasmic reticulum protein HSPA5/BiP is essential for decidual transformation of human endometrial stromal cells.Scientific reports · 2024Article
- Activation of Peroxisome Proliferator-Activated Receptor-β/δ (PPARβ/δ) in Keratinocytes by Endogenous Fatty Acids.Biomolecules · 2024Article
- Gain-of-Function p53N236S Mutation Drives the Bypassing of HRasInternational journal of molecular sciences · 2023Article
- Using mass spectrometry imaging to visualize age-related subcellular disruption.Frontiers in molecular biosciences · 2023Review
- [Research Progress on the Pathogenesis of Lung Cancer Associated with Idiopathic Pulmonary Fibrosis].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2022Review
- Review
- Down-regulation of AMPK/PPARδ signalling promotes endoplasmic reticulum stress-induced endothelial dysfunction in adult rat offspring exposed to maternal diabetes.Cardiovascular research · 2022Article
- Mechanisms and Regulation of Cellular Senescence.International journal of molecular sciences · 2021Review
- GRP78/BiP determines senescence evasion cell fate after cisplatin-based chemotherapy.Scientific reports · 2021Article
- PPARdelta in Affected Atopic Dermatitis and Psoriasis: A Possible Role in Metabolic Reprograming.International journal of molecular sciences · 2021Review
- PPAR Beta/Delta and the Hallmarks of Cancer.Cells · 2020Review
- The Emerging Role of PPAR Beta/Delta in Tumor Angiogenesis.PPAR research · 2020Review
- Regulatory mechanisms mediated by peroxisome proliferator-activated receptor-β/δ in skin cancer.Molecular carcinogenesis · 2019Review
- Idiopathic Pulmonary Fibrosis and Lung Cancer: Mechanisms and Molecular Targets.International journal of molecular sciences · 2019Review
- The nuclear receptor RXRA controls cellular senescence by regulating calcium signaling.Aging cell · 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
7 authors at 2 institutions in 1 country.
Funding
Abstract
Endoplasmic reticulum (ER) stress and ER stress-associated unfolded protein response (UPR) can promote cancer cell survival, but it remains unclear whether they can influence oncogene-induced senescence. The present study examined the role of ER stress in senescence using oncogene-dependent models. Increased ER stress attenuated senescence in part by up-regulating phosphorylated protein kinase B (p-AKT) and decreasing phosphorylated extracellular signal-regulated kinase (p-ERK). A positive feed forward loop between p-AKT, ER stress, and UPR was discovered whereby a transient increase of ER stress caused reduced senescence and promotion of tumorigenesis. Decreased ER stress was further correlated with increased senescence in both mouse and human tumors. Interestingly, H-RAS-expressing Pparβ/δ null cells and tumors having increased cell proliferation exhibited enhanced ER stress, decreased cellular senescence, and/or enhanced tumorigenicity. Collectively, these results demonstrate a new role for ER stress and UPR that attenuates H-RAS-induced senescence and suggest that PPARβ/δ can repress this oncogene-induced ER stress to promote senescence in accordance with its role as a tumor modifier that suppresses carcinogenesis.
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.