Marcela Teatin Latancia , Giovana da Silva Leandro , André Uchimura Bastos , Natália Cestari Moreno , Abu-Bakr Adetayo Ariwoola , Davi Jardim Martins , Nicholas William Ashton , Victória Chaves Ribeiro , Nicolas Carlos Hoch , Clarissa Ribeiro Reily Rocha , Roger Woodgate , Carlos Frederico Martins Menck
{"title":"人类转座DNA聚合酶ι和κ介导MGMT缺陷胶质母细胞瘤细胞对替莫唑胺的耐受性。","authors":"Marcela Teatin Latancia , Giovana da Silva Leandro , André Uchimura Bastos , Natália Cestari Moreno , Abu-Bakr Adetayo Ariwoola , Davi Jardim Martins , Nicholas William Ashton , Victória Chaves Ribeiro , Nicolas Carlos Hoch , Clarissa Ribeiro Reily Rocha , Roger Woodgate , Carlos Frederico Martins Menck","doi":"10.1016/j.dnarep.2024.103715","DOIUrl":null,"url":null,"abstract":"<div><p>Glioblastoma (GBM) is a highly aggressive brain tumor associated with poor patient survival. The current standard treatment involves invasive surgery, radiotherapy, and chemotherapy employing temozolomide (TMZ). Resistance to TMZ is, however, a major challenge. Previous work from our group has identified candidate genes linked to TMZ resistance, including genes encoding translesion synthesis (TLS) DNA polymerases iota (Polɩ) and kappa (Polκ). These specialized enzymes are known for bypassing lesions and tolerating DNA damage. Here, we investigated the roles of Polɩ and Polκ in TMZ resistance, employing MGMT-deficient U251-MG glioblastoma cells, with knockout of either <em>POLI</em> or <em>POLK</em> genes encoding Polɩ and Polκ, respectively, and assess their viability and genotoxic stress responses upon subsequent TMZ treatment. Cells lacking either of these polymerases exhibited a significant decrease in viability following TMZ treatment compared to parental counterparts. The restoration of the missing polymerase led to a recovery of cell viability. Furthermore, knockout cells displayed increased cell cycle arrest, mainly in late S-phase, and lower levels of genotoxic stress after TMZ treatment, as assessed by a reduction of γH2AX foci and flow cytometry data. This implies that TMZ treatment does not trigger a significant H2AX phosphorylation response in the absence of these proteins. Interestingly, combining TMZ with Mirin (double-strand break repair pathway inhibitor) further reduced the cell viability and increased DNA damage and γH2AX positive cells in TLS KO cells, but not in parental cells. These findings underscore the crucial roles of Polɩ and Polκ in conferring TMZ resistance and the potential backup role of homologous recombination in the absence of these TLS polymerases. Targeting these TLS enzymes, along with double-strand break DNA repair inhibition, could, therefore, provide a promising strategy to enhance TMZ's effectiveness in treating GBM.</p></div>","PeriodicalId":300,"journal":{"name":"DNA Repair","volume":"141 ","pages":"Article 103715"},"PeriodicalIF":3.0000,"publicationDate":"2024-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1568786424000910/pdfft?md5=5c94860c649134a2ff80bcadd7bc1372&pid=1-s2.0-S1568786424000910-main.pdf","citationCount":"0","resultStr":"{\"title\":\"Human translesion DNA polymerases ι and κ mediate tolerance to temozolomide in MGMT-deficient glioblastoma cells.\",\"authors\":\"Marcela Teatin Latancia , Giovana da Silva Leandro , André Uchimura Bastos , Natália Cestari Moreno , Abu-Bakr Adetayo Ariwoola , Davi Jardim Martins , Nicholas William Ashton , Victória Chaves Ribeiro , Nicolas Carlos Hoch , Clarissa Ribeiro Reily Rocha , Roger Woodgate , Carlos Frederico Martins Menck\",\"doi\":\"10.1016/j.dnarep.2024.103715\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Glioblastoma (GBM) is a highly aggressive brain tumor associated with poor patient survival. 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Furthermore, knockout cells displayed increased cell cycle arrest, mainly in late S-phase, and lower levels of genotoxic stress after TMZ treatment, as assessed by a reduction of γH2AX foci and flow cytometry data. This implies that TMZ treatment does not trigger a significant H2AX phosphorylation response in the absence of these proteins. Interestingly, combining TMZ with Mirin (double-strand break repair pathway inhibitor) further reduced the cell viability and increased DNA damage and γH2AX positive cells in TLS KO cells, but not in parental cells. These findings underscore the crucial roles of Polɩ and Polκ in conferring TMZ resistance and the potential backup role of homologous recombination in the absence of these TLS polymerases. 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引用次数: 0
摘要
胶质母细胞瘤(GBM)是一种侵袭性极强的脑肿瘤,患者生存率极低。目前的标准治疗包括侵入性手术、放疗和使用替莫唑胺(TMZ)的化疗。然而,TMZ 的抗药性是一大挑战。我们研究小组之前的研究发现了与 TMZ 耐药性相关的候选基因,包括编码转子合成(TLS)DNA 聚合酶 iota (Pol⚙) 和 kappa (Polκ) 的基因。这些专门的酶以绕过病变和耐受 DNA 损伤而闻名。在这里,我们利用MGMT缺陷的U251-MG胶质母细胞瘤细胞,分别敲除编码Polɩ和Polκ的POLI或POLK基因,研究了Polɩ和Polκ在TMZ抗性中的作用,并评估了它们在随后的TMZ处理中的活力和基因毒性应激反应。与亲代细胞相比,缺失这两种聚合酶的细胞在接受 TMZ 处理后的存活率明显下降。恢复缺失的聚合酶后,细胞活力得以恢复。此外,基因敲除细胞在 TMZ 处理后表现出细胞周期停滞(主要是晚期 S 期)和较低的基因毒性应激水平,这可以通过减少 γH2AX 病灶和流式细胞术数据来评估。这意味着在没有这些蛋白的情况下,TMZ 处理不会引发明显的 H2AX 磷酸化反应。有趣的是,将 TMZ 与 Mirin(双链断裂修复途径抑制剂)结合使用会进一步降低 TLS KO 细胞的细胞活力,增加 DNA 损伤和 γH2AX 阳性细胞,而亲代细胞则不会。这些发现强调了Polɩ和Polκ在赋予TMZ抗性中的关键作用,以及在缺乏这些TLS聚合酶的情况下同源重组的潜在后备作用。因此,以这些 TLS 酶为靶点,同时抑制双链断裂 DNA 修复,可为提高 TMZ 治疗 GBM 的疗效提供一种前景广阔的策略。
Human translesion DNA polymerases ι and κ mediate tolerance to temozolomide in MGMT-deficient glioblastoma cells.
Glioblastoma (GBM) is a highly aggressive brain tumor associated with poor patient survival. The current standard treatment involves invasive surgery, radiotherapy, and chemotherapy employing temozolomide (TMZ). Resistance to TMZ is, however, a major challenge. Previous work from our group has identified candidate genes linked to TMZ resistance, including genes encoding translesion synthesis (TLS) DNA polymerases iota (Polɩ) and kappa (Polκ). These specialized enzymes are known for bypassing lesions and tolerating DNA damage. Here, we investigated the roles of Polɩ and Polκ in TMZ resistance, employing MGMT-deficient U251-MG glioblastoma cells, with knockout of either POLI or POLK genes encoding Polɩ and Polκ, respectively, and assess their viability and genotoxic stress responses upon subsequent TMZ treatment. Cells lacking either of these polymerases exhibited a significant decrease in viability following TMZ treatment compared to parental counterparts. The restoration of the missing polymerase led to a recovery of cell viability. Furthermore, knockout cells displayed increased cell cycle arrest, mainly in late S-phase, and lower levels of genotoxic stress after TMZ treatment, as assessed by a reduction of γH2AX foci and flow cytometry data. This implies that TMZ treatment does not trigger a significant H2AX phosphorylation response in the absence of these proteins. Interestingly, combining TMZ with Mirin (double-strand break repair pathway inhibitor) further reduced the cell viability and increased DNA damage and γH2AX positive cells in TLS KO cells, but not in parental cells. These findings underscore the crucial roles of Polɩ and Polκ in conferring TMZ resistance and the potential backup role of homologous recombination in the absence of these TLS polymerases. Targeting these TLS enzymes, along with double-strand break DNA repair inhibition, could, therefore, provide a promising strategy to enhance TMZ's effectiveness in treating GBM.
期刊介绍:
DNA Repair provides a forum for the comprehensive coverage of DNA repair and cellular responses to DNA damage. The journal publishes original observations on genetic, cellular, biochemical, structural and molecular aspects of DNA repair, mutagenesis, cell cycle regulation, apoptosis and other biological responses in cells exposed to genomic insult, as well as their relationship to human disease.
DNA Repair publishes full-length research articles, brief reports on research, and reviews. The journal welcomes articles describing databases, methods and new technologies supporting research on DNA repair and responses to DNA damage. Letters to the Editor, hot topics and classics in DNA repair, historical reflections, book reviews and meeting reports also will be considered for publication.