ArticleCell death discovery2026
Targeting common denominators of DNA damage tolerance mechanisms as therapeutic strategy to cope with dynamic phenotypic changes in triple-negative breast cancer cells.
Article in Cell death discovery, 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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11 authors.
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Abstract
Triple negative breast cancer (TNBC) is the most aggressive type of breast cancer with limited treatment options and a propensity towards chemoresistance. Given the lack of targetable receptors, treatment relies primarily on chemotherapy. While mechanisms leading to chemoresistance are vastly unknown, DNA damage tolerance (DDT) pathways have emerged as potential drivers of chemoresistance. Herein, we report a phenotypic characterization of four TNBC- and six non-TNBC cell lines, which supports the relevance of DDT in the TNBC response to chemotherapy. We unveiled an association between DDT pathway activation through PCNA-ubiquitination, augmented epithelial-to-mesenchymal transition (EMT) and stemness features, specifically in 3D spheroid culture from TNBC cells. Analysis of replication dynamics revealed a pronounced replication slowdown in 3D- versus 2D-cultured TNBC but not in non-TNBC cells. The exploration of DDT pathway usage in three TNBC cell lines (MDA-MB-231, Hs578t, MDA-MB-468) uncovers reliance on ZRANB3-, HLTF- and SMARCAL1-dependent fork reversal in 3D, while translesion DNA synthesis (TLS) polymerases (POLs) were more active under 2D conditions. Screening cytotoxicity with a panel of ten drugs targeting key DDT pathway components identified POLζ inhibition (JH-RE-06; IC
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