Ubiquitin-Mediated Control of ETS Transcription Factors: Roles in Cancer and Development

Ducker, Charles; Shaw, Peter E.

doi:10.3390/ijms22105119

Cited by 11 publications

(6 citation statements)

References 119 publications

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“…We observed an increased expression of Spdef throughout the time-course of CGNs apoptosis and its down-regulation following NFs treatment ( Figure 1 and Figure 3 ) [ 43 ]. This evidence supports previous studies proposing its role as a tumor suppressor in various types of cancers [ 186 , 187 ]. In addition, altered expression of SPDEF has been found in Alzheimer’s disease patients and animal models, while a recent association was found between blood-based Spdef methylation and stress response, altered dopaminergic neurotransmission and increased vulnerability to substance abuse, suggesting its role as a biomarker for these pathological conditions [ 188 , 189 , 190 , 191 ].…”

Section: Cracking the Transcriptional Regulatory Programs Of Neuronal...supporting

confidence: 92%

Cracking the Code of Neuronal Cell Fate

Morello

Cognata

Guarnaccia

et al. 2023

Cells

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Transcriptional regulation is fundamental to most biological processes and reverse-engineering programs can be used to decipher the underlying programs. In this review, we describe how genomics is offering a systems biology-based perspective of the intricate and temporally coordinated transcriptional programs that control neuronal apoptosis and survival. In addition to providing a new standpoint in human pathology focused on the regulatory program, cracking the code of neuronal cell fate may offer innovative therapeutic approaches focused on downstream targets and regulatory networks. Similar to computers, where faults often arise from a software bug, neuronal fate may critically depend on its transcription program. Thus, cracking the code of neuronal life or death may help finding a patch for neurodegeneration and cancer.

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Section: Cracking the Transcriptional Regulatory Programs Of Neuronal...supporting

confidence: 92%

Cracking the Code of Neuronal Cell Fate

Morello

Cognata

Guarnaccia

et al. 2023

Cells

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show abstract

“…The E-twenty-six/E26 (ETS) family genes were originally discovered within the erythroleukemia-causing avian retrovirus E26 through the viral ets ( v-ets ) oncogene, which was found to have been transduced from homologous genes in the chicken genome to encode part of a hybrid viral protein [ 43 ]. ETS transcription factors contain a highly conserved ETS DNA-binding domain that interacts together with other transcription factors to enhance the elements [ 44 ].…”

Section: Molecular Biology and Genomic Features Of Aelmentioning

confidence: 99%

Acute Erythroid Leukemia: From Molecular Biology to Clinical Outcomes

Fernandes,

Waldron,

Chatzilygeroudi

et al. 2024

IJMS

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Acute Erythroid Leukemia (AEL) is a rare and aggressive subtype of Acute Myeloid Leukemia (AML). In 2022, the World Health Organization (WHO) defined AEL as a biopsy with ≥30% proerythroblasts and erythroid precursors that account for ≥80% of cellularity. The International Consensus Classification refers to this neoplasm as “AML with mutated TP53”. Classification entails ≥20% blasts in blood or bone marrow biopsy and a somatic TP53 mutation (VAF > 10%). This type of leukemia is typically associated with biallelic TP53 mutations and a complex karyotype, specifically 5q and 7q deletions. Transgenic mouse models have implicated several molecules in the pathogenesis of AEL, including transcriptional master regulator GATA1 (involved in erythroid differentiation), master oncogenes, and CDX4. Recent studies have also characterized AEL by epigenetic regulator mutations and transcriptome subgroups. AEL patients have overall poor clinical outcomes, mostly related to their poor response to the standard therapies, which include hypomethylating agents and intensive chemotherapy. Allogeneic bone marrow transplantation (AlloBMT) is the only potentially curative approach but requires deep remission, which is very challenging for these patients. Age, AlloBMT, and a history of antecedent myeloid neoplasms further affect the outcomes of these patients. In this review, we will summarize the diagnostic criteria of AEL, review the current insights into the biology of AEL, and describe the treatment options and outcomes of patients with this disease.

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“…Lysine-380 is located within the DNA-binding domain and is also present in wild-type FLI1 and conserved in several other members of the ETS family like ETS1. However, this may limit specificity [107]. Although, given the short half-life of EWSR-FLI1, a PROTAC targeting a lysine-380-containing motif could create a therapeutic window [106].…”

Section: Combining Targeted Drugs With Protein Degradationmentioning

confidence: 99%

Drug Targeting of Chromosomal Translocations in Fusion-Positive Sarcoma

Richter¹

2023

Bone Tumours - A Comprehensive Review of Selected Topics

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Sarcomas are heterogeneous cancers of bone or soft tissue. They occur in children, adolescents, and young adults (AYAs). Herein, the subgroup of fusion-positive (FP) sarcomas is characterized by chromosomal rearrangements generating pathognomonic fusion transcripts and oncoproteins. In Ewing sarcoma (EwS), FP-rhabdomyosarcomas (FP-RMS) and synovial sarcomas (SyS), the most common and aggressive forms of sarcomas in childhood and adolescence, the oncogenic rearrangements involve transcription cofactors such as by FET-ETS, PAX3/7-FOXO1 or SS18-SSX fusion oncogenes in EwS, FP-RMS, or SyS, respectively causing widespread epigenetic rewiring and aberrant gene expression. Regardless of these translocations, few recurrent mutations are observed in these sarcomas that may contribute to disease; thus, it is of particular interest to consider the consequences of these translocations for tumor development. Results of current research examining the disease, analyzing, and classifying the role of associated rearrangements of chromatin, and investigating possibilities for tumor-specific intervention such as blocking the transcriptional activity of the fusion protein, or the processes caused by this activity are summarized here and some resulting therapeutic opportunities are presented.

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Ubiquitin-Mediated Control of ETS Transcription Factors: Roles in Cancer and Development

Cited by 11 publications

References 119 publications

Cracking the Code of Neuronal Cell Fate

Cracking the Code of Neuronal Cell Fate

Acute Erythroid Leukemia: From Molecular Biology to Clinical Outcomes

Drug Targeting of Chromosomal Translocations in Fusion-Positive Sarcoma

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