ArticleNucleus (Austin, Tex.)2026
Repair and misrepair of telomeric DNA in dynamic interactions with PML nuclear bodies and lamin B1 in doxorubicin-treated cancer cells.
Article in Nucleus (Austin, Tex.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Telomeres in epithelial tumors are maintained by telomerase; however, in the MDA-MB-231 breast cancer cell line, treated by doxorubicin (DOX), we found a transient suppression of the telomerase (TERT) before cell growth resumed. Accumulation of cells in late-S-G2/M, mitotic slippage, octaploidy, and decrease of lamin B1 (LMNB1) coincided with this response. The telomere clustering and ALT-like process marked by the telomere shelterin (TRF2) colocalised in PML bodies with DNA DSBs (γH2AX) and recombinase RAD51 were observed in 11-12% of cells. They were preset by arrays of PML-bodies juxta-colocalized with the foci of meiotic prophase proteins SPO11 and DMC1. On the 3rd week, the cells de-polyploidised and returned to the normal cycle, telomerase, and mitosis. ALT-like bodies were also found in BRAFV600E-SK-MEL-28 DOX-treated melanoma cells. However, after sublethal doses of DOX, the formation of PML dimeric rods flanked and tandemly joined by misrepaired TRF2/γH2AX foci occured. Such PML tracts, circumventing cell nuclei undergoing MOS-microtubule-driven rotation, interacted with peripheral chromatin and intermitted with LMNB1 fragments. Furthermore, LMNB1 massively left the nuclear periphery, forming intranuclear flows, and/or convoluted into large peri-nucleolar PML bodies. We interpret our observations as the attempts by damaged, senescing cancer cells to use several mechanisms exploiting PML isoforms and meiotic proteins for telomere repair.
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