ArticleBMC cell biology2010
3D nuclear organization of telomeres in the Hodgkin cell lines U-HO1 and U-HO1-PTPN1: PTPN1 expression prevents the formation of very short telomeres including "t-stumps".
Article in BMC cell biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Review
- Single-Run Catalysis and Kinetic Control of Human Telomerase Holoenzyme.Advances in experimental medicine and biology · 2022Review
- The PTP1B mutant PTP1B∆2-4 is a positive regulator of the JAK/STAT signalling pathway in Hodgkin lymphoma.Carcinogenesis · 2021Article
- The Transition between Telomerase and ALT Mechanisms in Hodgkin Lymphoma and Its Predictive Value in Clinical Outcomes.Cancers · 2018Article
- Review
- Telomere Homeostasis: Interplay with Magnesium.International journal of molecular sciences · 2018Review
- Identification of Neuroblastoma Subgroups Based on Three-Dimensional Telomere Organization.Translational oncology · 2016Article
- CK1δ in lymphoma: gene expression and mutation analyses and validation of CK1δ kinase activity for therapeutic application.Frontiers in cell and developmental biology · 2015Article
- Differences in nuclear DNA organization between lymphocytes, Hodgkin and Reed-Sternberg cells revealed by structured illumination microscopy.Journal of cellular biochemistry · 2014Article
- Three-dimensional Nuclear Telomere Organization in Multiple Myeloma.Translational oncology · 2013Article
- Three-dimensional nuclear telomere architecture changes during endometrial carcinoma development.Genes, chromosomes & cancer · 2013Article
- Genomic Instability: The Driving Force behind Refractory/Relapsing Hodgkin's Lymphoma.Cancers · 2013Article
- The kelch protein KLHDC8B guards against mitotic errors, centrosomal amplification, and chromosomal instability.The Journal of biological chemistry · 2012Article
- Three-dimensional Telomere Signatures of Hodgkin- and Reed-Sternberg Cells at Diagnosis Identify Patients with Poor Response to Conventional Chemotherapy.Translational oncology · 2012Article
- Selected telomere length changes and aberrant three-dimensional nuclear telomere organization during fast-onset mouse plasmacytomas.Neoplasia (New York, N.Y.) · 2012Article
- Telomeres and viruses: common themes of genome maintenance.Frontiers in oncology · 2012Article
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8 authors at 3 institutions in 2 countries.
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Abstract
backgroundIn cancer cells the three-dimensional (3D) telomere organization of interphase nuclei into a telomeric disk is heavily distorted and aggregates are found. In Hodgkin's lymphoma quantitative FISH (3D Q-FISH) reveals a major impact of nuclear telomere dynamics during the transition form mononuclear Hodgkin (H) to diagnostic multinuclear Reed-Sternberg (RS) cells. In vitro and in vivo formation of RS-cells is associated with the increase of very short telomeres including "t-stumps", telomere loss, telomeric aggregate formation and the generation of "ghost nuclei".
resultsHere we analyze the 3D telomere dynamics by Q-FISH in the novel Hodgkin cell line U-HO1 and its non-receptor protein-tyrosine phosphatase N1 (PTPN1) stable transfectant U-HO1-PTPN1, derived from a primary refractory Hodgkin's lymphoma. Both cell lines show equally high telomerase activity but U-HO1-PTPN differs from U-HO1 by a three times longer doubling time, low STAT5A expression, accumulation of RS-cells (p < 0.0001) and a fourfold increased number of apoptotic cells.As expected, multinuclear U-HO1-RS-cells and multinuclear U-HO1-PTPN1-RS-cells differ from their mononuclear H-precursors by their nuclear volume (p < 0.0001), the number of telomeres (p < 0.0001) and the increase in telomere aggregates (p < 0.003). Surprisingly, U-HO1-RS cells differ from U-HO1-PTPN1-RS-cells by a highly significant increase of very short telomeres including "t-stumps" (p < 0.0001).
conclusionAbundant RS-cells without additional very short telomeres including "t-stumps", high rate of apoptosis, but low STAT5A expression, are hallmarks of the U-HO1-PTPN1 cell line. These characteristics are independent of telomerase activity. Thus, PTPN1 induced dephosphorylation of STAT5 with consecutive lack of Akt/PKB activation and cellular arrest in G₂, promoting induction of apoptosis, appears as a possible pathogenetic mechanism deserving further experimental investigation.
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