ArticleChemico-biological interactions2025
Four germline POLH variants, including two found in skin tumors, impair DNA polymerase η function and cellular tolerance to UV radiation and cisplatin.
Article in Chemico-biological interactions, 2025. 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
DNA polymerase (pol) η is vital for accurately replicating DNA opposite ultraviolet light (UV)-induced cyclobutane pyrimidine dimers and cisplatin-induced intrastrand purine crosslinks. While human POLH deficiency is linked to the disease xeroderma pigmentosum variant, the functional consequences of germline and somatic POLH variants remain largely unexplored. We characterized nine nonsynonymous POLH germline variants, five of which have also been found in various tumors. Enzyme activity was first assessed using recombinant pol η (residues 1-432) proteins. Variants F17S, C227Y, and R356X displayed substantially reduced or nearly abolished polymerase activity opposite cis-syn cyclobutane thymine dimer (CTD) compared to the wild-type. Cellular effects were then evaluated in POLH-deficient human embryonic kidney (HEK) 293 cells. Unlike cells transfected with wild-type POLH, cells transfected with F17S, R81C, C227Y, or R356X variants failed to rescue UV- and cisplatin-sensitivity. Interestingly, the R81C variant protein was undetectable in transfected cells. Further steady-state kinetic analysis revealed that the F17S, C227Y, and R356X variants had 3- to 5000-fold reductions in k
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