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The antineoplastic agent streptozotocin induces short-term telomere instability in Epstein-Barr virus-transformed human lymphoblastoid cells
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DOI：10.1016/j.yexcr.2026.114998.png)
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Abstract
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We assessed the induction of telomere instability-related chromosomal aberrations by streptozotocin (STZ) in human lymphoblastoid cells (T-37) immortalized with Epstein-Barr virus (EBV) using Peptide Nucleic Acid-Fluorescence In Situ Hibridization (PNA-FISH) with pan-telomeric and pan-centromeric probes. Cells were exposed to STZ at concentrations ranging from 0.5 to 4.0 mM in sodium citrate (SC, pH 4.4) for 1 h at 37 degrees C, and chromosomal aberrations were analyzed 24 h later. Incomplete chromosome elements (ICE) significantly increased after STZ treatments at 2 and 4 mM compared to untreated and SC-treated cultures (p < 0.05). The total number of telomeric signals lost (TSL) and the frequency of chromosome-type telomere signal loss per cell rose significantly after STZ treatments of 0.5 and 1 mM compared to untreated and SC-treated cultures (p < 0.05). Both SC and STZ caused chromatid-type telomere signal loss and duplications (TSD), but differences between these treatments were non-significant (p > 0.05). Non-significant differences between treatments in terms of telomere fusions, associations, ectopic signals, or sister-chromatid telomere fusions were observed (p > 0.05). Quantitative FISH (Q-FISH) revealed longer telomeres in cells treated with SC (10 and 60 mu L) or STZ (0.5, 1, and 3 mM) compared to untreated cells (p < 0.05), with non-significant differences between SC and STZ (p > 0.05). These results indicate that STZ induces short-term telomere instability, while suggest that SC induces telomere dysfunction and elongation in human lymphoblastoid cells.
Keywords:
Chromosome end loss
Telomere aberrations
Telomere dysfunction
Telomere elongation
PNA-FISH
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