P53: A key player in diverse cellular processes including nuclear stress and ribosome biogenesis, highlighting potential therapeutic compounds

Temaj, Gazmend; Chichiarelli, Silvia; Telkoparan-Akillilar, Pelin; Saha, Sarmistha; Nuhii, Nexhibe; Hadziselimovic, Rifat; Saso, Luciano

doi:10.1016/j.bcp.2024.116332

Biochemical Pharmacology

2024

DOI: 10.1016/j.bcp.2024.116332

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P53: A key player in diverse cellular processes including nuclear stress and ribosome biogenesis, highlighting potential therapeutic compounds

Gazmend Temaj,

Silvia Chichiarelli,

Pelin Telkoparan-Akillilar

et al.

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Cited by 3 publications

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Ribosomal rodeo: wrangling translational machinery in gynecologic tumors

Filipek,

Penzo

2024

Cancer Metastasis Rev

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Gynecologic cancers are a significant cause of morbidity and mortality among women worldwide. Despite advancements in diagnosis and treatment, the molecular mechanisms underlying the development and progression of these cancers remain poorly understood. Recent studies have implicated translational machinery (ribosomal proteins (RPs) and translation factors (TFs)) as potential drivers of oncogenic processes in various cancer types, including gynecologic cancers. RPs are essential components of the ribosome, which is responsible for protein synthesis. In this review paper, we aim to explore the role of translational machinery in gynecologic cancers. Specifically, we will investigate the potential mechanisms by which these components contribute to the oncogenic processes in these cancers and evaluate the feasibility of targeting RPs as a potential therapeutic strategy. By doing so, we hope to provide a broader view of the molecular pathogenesis of gynecologic cancers and highlight their potential as novel therapeutic targets for the management of these challenging diseases.

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Ribosomal rodeo: wrangling translational machinery in gynecologic tumors

Filipek,

Penzo

2024

Cancer Metastasis Rev

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Ultrarare Variants in DNA Damage Repair Genes in Pediatric Acute-Onset Neuropsychiatric Syndrome or Acute Behavioral Regression in Neurodevelopmental Disorders

Cunningham,

Frankovich,

Dubin

et al. 2024

Dev Neurosci

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Acute onset of severe psychiatric symptoms or regression may occur in children with premorbid neurodevelopmental disorders, although typically developing children can also be affected. Infections or other stressors are likely triggers. The underlying causes are unclear, but a current hypothesis suggests the convergence of genes that influence neuronal and immunological function. We previously identified 11 genes in Pediatric Acute-Onset Neuropsychiatry Syndrome (PANS), in which two classes of genes related to either synaptic function or the immune system were found. Among the latter, three affect the DNA damage response (DDR): PPM1D, CHK2, and RAG1. We now report an additional 17 cases with mutations in PPM1D and other DDR genes in patients with acute onset of psychiatric symptoms and/or regression that their clinicians classified as PANS or another inflammatory brain condition. The genes include clusters affecting p53 DNA repair (PPM1D, ATM, ATR, 53BP1, and RMRP), and the Fanconi Anemia Complex (FANCE, SLX4/FANCP, FANCA, FANCI, and FANCC). We hypothesize that defects in DNA repair genes, in the context of infection or other stressors, could contribute to decompensated states through an increase in genomic instability with a concomitant accumulation of cytosolic DNA in immune cells triggering DNA sensors, such as cGAS-STING and AIM2 inflammasomes, as well as central deficits on neuroplasticity. In addition, increased senescence and defective apoptosis affecting immunological responses could be playing a role. These compelling preliminary findings motivate further genetic and functional characterization as the downstream impact of DDR deficits may point to novel treatment strategies.

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The Interplay Between the MYC Oncogene and Ribosomal Proteins in Osteosarcoma Onset and Progression: Potential Mechanisms and Indication of Candidate Therapeutic Targets

Guerrieri,

Hattinger,

Marchesini

et al. 2024

IJMS

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High-grade osteosarcoma (OS) is the most common primary bone tumor mainly affecting children and young adults. First-line treatment consists of neo-adjuvant chemotherapy with doxorubicin, cisplatin, and methotrexate and surgery. The mean long-term survival rate for localized disease at diagnosis is 65–70%, dropping down to 20% when metastases are present at diagnosis. Therefore, curing OS is a clinical challenge, particularly for patients that do not respond to standard treatments. MYC has frequently been reported to be involved in the pathogenesis of OS and its high expression may be associated with drug resistance and patients’ worse prognosis. Moreover, MYC is a master regulator of ribosomal proteins (RPs) synthesis and ribosome biogenesis (RiBi), which is often up-regulated in human tumors. In recent years, RPs have been recognized not only for their traditional role in ribosome assembly but also for their extra-ribosomal functions, many of which are linked to the onset and progression of cancer. In this review we focus on the role and possible interplay of MYC and RPs expression in association with drug resistance and worse prognosis in OS and discuss therapeutic options that target de-regulated MYC, RiBi, or RPs, which are already clinically available or under evaluation in clinical trials.

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P53: A key player in diverse cellular processes including nuclear stress and ribosome biogenesis, highlighting potential therapeutic compounds

Cited by 3 publications

References 208 publications

Ribosomal rodeo: wrangling translational machinery in gynecologic tumors

Ribosomal rodeo: wrangling translational machinery in gynecologic tumors

Ultrarare Variants in DNA Damage Repair Genes in Pediatric Acute-Onset Neuropsychiatric Syndrome or Acute Behavioral Regression in Neurodevelopmental Disorders

The Interplay Between the MYC Oncogene and Ribosomal Proteins in Osteosarcoma Onset and Progression: Potential Mechanisms and Indication of Candidate Therapeutic Targets

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