ArticleOncotarget2016
PIM1 destabilization activates a p53-dependent response to ribosomal stress in cancer cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- A systematic review on active sites and functions of PIM-1 protein.Human cell · 2022Pooled it
- The Nucleolus in Human Disease: Ribosome Biogenesis, Nucleolar Surveillance, and Therapeutic Opportunities.Biomolecules · 2026Review
- PIM kinase inhibition counters resistance to radiotherapy and chemotherapy in human prostate cancer.Radiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology · 2025Article
- Pim1 promotes the maintenance of bone homeostasis by regulating osteoclast function.Experimental & molecular medicine · 2025Article
- An RPS19-edited model for Diamond-Blackfan anemia reveals TP53-dependent impairment of hematopoietic stem cell activity.JCI insight · 2023Article
- Inflammatory bowel disease induces inflammatory and pre-neoplastic changes in the prostate.Prostate cancer and prostatic diseases · 2022Article
- Correction: Inflammatory bowel disease induces inflammatory and preneoplastic changes in the prostate.Prostate cancer and prostatic diseases · 2022Article
- PIM1 Inhibition Affects Glioblastoma Stem Cell Behavior and Kills Glioblastoma Stem-like Cells.International journal of molecular sciences · 2021Article
- Integrative proteomics reveals principles of dynamic phosphosignaling networks in human erythropoiesis.Molecular systems biology · 2020Article
- Histone methyltransferase DOT1L coordinates AR and MYC stability in prostate cancer.Nature communications · 2020Article
- EPHB4 inhibition activates ER stress to promote immunogenic cell death of prostate cancer cells.Cell death & disease · 2019Article
- Shaping the regulation of the p53 mRNA tumour suppressor: the co-evolution of genetic signatures.BMC cancer · 2019Review
- Rare syndromes of the head and face: mandibulofacial and acrofacial dysostoses.Wiley interdisciplinary reviews. Developmental biology · 2017Review
- Depletion of ribosomal protein S19 causes a reduction of rRNA synthesis.Scientific reports · 2016Article
- Nucleolus-derived mediators in oncogenic stress response and activation of p53-dependent pathways.Histochemistry and cell biology · 2016Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Defects in ribosome biogenesis triggers a stress response (ribosomal stress) that can lead to growth arrest and apoptosis. Signaling pathways activated by ribosomal stress are specifically involved in the pathological mechanism of a group of disorders defined as ribosomopathies. However, more generally, the quality control of ribosome synthesis is part of the regulatory circuits that control cell metabolism. A number of studies identified tumor suppressor p53 as a central player in ribosomal stress. We have previously reported that the kinase PIM1 plays a role as a sensor for ribosome deficiency. In this report we address the relationship between PIM1 and p53 in cancer cell lines after depletion of a ribosomal protein. We identified a novel signaling pathway that includes the kinase AKT and the ubiquitin ligase MDM2. In fact, our results indicate that the lower level of PIM1, induced by ribosomal stress, causes inactivation of AKT, inhibition of MDM2 and a consequent p53 stabilization. Therefore, we propose that activation of p53 in response to ribosomal stress, is dependent on the pathway PIM1-AKT-MDM2. In addition, we report evidence that PIM1 level may be relevant to assess the sensitivity of cancer cells to chemotherapeutic drugs that induce ribosomal stress.
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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.