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More than 50% of prostate tumors have a chromosomal rearrangement resulting in aberrant expression of an oncogenic ETS family transcription factor. However, mechanisms that differentiate the function of oncogenic ETS factors expressed in prostate tumors from non-oncogenic ETS factors expressed in normal prostate are unknown. Here, we find that four oncogenic ETS (ERG, ETV1, ETV4, and ETV5), and no other ETS, interact with the Ewing's sarcoma breakpoint protein, EWS. This EWS interaction was necessary and sufficient for oncogenic ETS functions including gene activation, cell migration, clonogenic survival, and transformation. Significantly, the EWS interacting region of ERG has no homology with that of ETV1, ETV4, and ETV5. Therefore, this finding may explain how divergent ETS factors have a common oncogenic function. Strikingly, EWS is fused to various ETS factors by the chromosome translocations that cause Ewing's sarcoma. Therefore, these findings link oncogenic ETS function in both prostate cancer and Ewing's sarcoma.
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http://dx.doi.org/10.1016/j.celrep.2016.10.001 | DOI Listing |
Dev Cell
September 2025
Division of Surgical Sciences, Department of Surgery, UC San Diego Health, 3855 Health Sciences Drive, La Jolla, CA 92037, USA. Electronic address:
In this issue of Developmental Cell, Li et al. show that ETS variant transcription factor 1 (Etv1) SUMOylation not only maintains cancer stem cells (CSCs) but also enables their communications with non-CSC cancer cells to induce tumorigenesis of non-CSCs. The finding reveals a new function of CSCs in driving aggressive tumorigenesis that is SUMOylation dependent.
View Article and Find Full Text PDFMedicine (Baltimore)
September 2025
Department of Medicine, Ibn e Seena Hospital, Kabul, Afghanistan.
The ETS2 gene, a member of the ETS (E26 transformation-specific) family of transcription factors, plays a critical role in the regulation of immune responses, epithelial barrier integrity, and fibrosis, all of which are central to the pathogenesis of inflammatory bowel disease (IBD). This review explores the molecular characteristics of ETS2, its involvement in immune dysregulation, and its contribution to IBD-associated complications, including fibrosis and colorectal cancer. ETS2 regulates key inflammatory pathways such as NF-κB and JAK-STAT, influencing cytokine production and immune cell polarization.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
August 2025
Laboratory of Molecular Biology, Research Centre for Medical Genetics (RCMG), 115522 Moscow, Russia.
Background: Schizophrenia (SZ) is associated with chronic oxidative stress in the patient's body. Previous studies revealed an increased copy number of genes for 47S pre-ribosomal RNA (pre-rRNA) in SZ patients. In this study, levels of oxidative stress and factors involved in the adaptive response to chronic stress (rDNA transcription) were, for the first time, compared in blood cells of patients with catatonic SZ(C) and paranoid SZ(P), chronic forms of schizophrenia, as well as healthy controls (HC).
View Article and Find Full Text PDFNan Fang Yi Ke Da Xue Xue Bao
August 2025
Department of Pathogenic Biology & Key Laboratory of Tropical Translational Medicine of Ministry of Education, School of Basic Medicine and Life Sciences, Hainan Medical University. Haikou 571199, China.
Objectives: To elucidate the anti-aging effect of β-sitosterol (BS), an important component in the fruits of Miq., in and its regulatory effect on ETS-5 gene to modulate ferroptosis.
Methods: treated with 10 µg/mL BS were monitored for survival time and changes in body length, motility, and reproductive function.
Nat Aging
September 2025
IFOM-ETS, The AIRC Institute of Molecular Oncology, Milan, Italy.
Aging is the main risk factor for Parkinson's disease (PD), yet our understanding of how age-related mechanisms contribute to PD pathophysiology remains limited. We conducted a longitudinal analysis of blood samples from the Parkinson's Progression Markers Initiative cohort to investigate DNA damage in PD. Patients with PD exhibited disrupted DNA repair pathways and biased suppression of longer transcripts, indicating age-related, transcription-stalling DNA damage.
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