Platinum complexes as inhibitors of DNA repair protein Ku70 and topoisomerase IIα in cancer cells

Wang, Xiaoyong; Zhang, Hongmei; Wang, Yanqing; Wang, Ying; Han, Qianqian; Yan, Honghao; Yang, Tao; Guo, Zijian

doi:10.1039/d1dt03700e

Cited by 4 publications

(3 citation statements)

References 50 publications

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“…Emerging combinatorial approaches involving platinum (II) complexes, e.g., [PtCl (NH3)2(9-(pyridin-2-ylmethyl)-9H-carbazole)]NO3 (OPPC), [PtCl(NH3)2(9-(pyridin-3ylmethyl)-9H-carbazole)]NO3 (MPPC), and [PtCl(NH3)2(9-(pyridin-4-ylmethyl)-9Hcarbazole)]NO3 (PPPC), targeting the DNA repair proteins Ku70 and TOPII were effective [184]. Additionally, 2-Amino-Pyrrole-Carboxylate (2-APC) amplifies doxorubicin (DOX) cytotoxicity by inhibiting DNA damage repair via Rad51 recombinase reduction.…”

Section: Dna Damage Response Pathways and Topo-active Drug Resistancementioning

confidence: 99%

Understanding Cancer’s Defense against Topoisomerase-Active Drugs: A Comprehensive Review

Sharma,

Bahot,

Sekar

et al. 2024

Cancers

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In recent years, the emergence of cancer drug resistance has been one of the crucial tumor hallmarks that are supported by the level of genetic heterogeneity and complexities at cellular levels. Oxidative stress, immune evasion, metabolic reprogramming, overexpression of ABC transporters, and stemness are among the several key contributing molecular and cellular response mechanisms. Topo-active drugs, e.g., doxorubicin and topotecan, are clinically active and are utilized extensively against a wide variety of human tumors and often result in the development of resistance and failure to therapy. Thus, there is an urgent need for an incremental and comprehensive understanding of mechanisms of cancer drug resistance specifically in the context of topo-active drugs. This review delves into the intricate mechanistic aspects of these intracellular and extracellular topo-active drug resistance mechanisms and explores the use of potential combinatorial approaches by utilizing various topo-active drugs and inhibitors of pathways involved in drug resistance. We believe that this review will help guide basic scientists, pre-clinicians, clinicians, and policymakers toward holistic and interdisciplinary strategies that transcend resistance, renewing optimism in the ongoing battle against cancer.

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Section: Dna Damage Response Pathways and Topo-active Drug Resistancementioning

confidence: 99%

Understanding Cancer’s Defense against Topoisomerase-Active Drugs: A Comprehensive Review

Sharma,

Bahot,

Sekar

et al. 2024

Cancers

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“…There is emerging combinatorial approaches to target DNA repair proteins such as Ku70 and Topo II as effective anticancer approaches by designing platinum (II) complexes such as [PtCl(NH3)2(9-(pyridin-2-ylmethyl)-9H-carbazole)]NO3 (OPPC), [PtCl(NH3)2(9-(pyridin-3ylmethyl)-9H-carbazole)]NO3 (MPPC), and [PtCl(NH3)2(9-(pyridin-4-ylmethyl)-9H-carbazole)]NO3 (PPPC) [184]. 2-Amino-Pyrrole-Carboxylate (2-APC) dramatically increases doxorubicin cytotoxicity and promotes apoptosis in cancer cells at non-toxic concentrations.…”

Section: Dna Damage Response Pathways and Topo-active Drug Resistancementioning

confidence: 99%

Cracking the Code: Understanding Cancer’s Defense against Topoisomerase-Active Drugs: A Comprehensive Review

Sinha

2023

Preprint

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In recent years, the emergence of cancer drug resistance is one of the crucial tumor hallmarks which is supported by the level of genetic heterogeneity and complexities at cellular levels. Oxidative stress, immune evasion, metabolic reprogramming, overexpression of ABC transporters and stemness are among the several key contributing molecular and cellular response mechanisms. Topo-active drugs, e.g., doxorubicin and topotecan, are clinically active and are utilized extensively against a wide variety of human tumors and often results in the development of resistance and failure to therapy. Thus, there is an urgent need for an incremental and comprehensive understanding of mechanisms of cancer drug resistance specifically in the context of topo-active drugs. This review delves into the intricate mechanistic aspects of these intracellular and extracellular topo-active drug resistance mechanisms and explores use of potential combinatorial approaches by utilizing various topo-active drugs and inhibitors of pathways involved in drug resistance. We believe that this review will help guide basic scientists, pre-clinicians, clinicians, and policymakers toward holistic and interdisciplinary strategies that transcend resistance, renewing optimism in the ongoing battle against cancer.

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“…1 Unfortunately, platinum drugs have serious dose-limiting toxic side effects including nephrotoxicity, ototoxicity, cardiotoxicity, neurotoxicity, and systemic toxicity has caused serious damage to patients. [2][3][4][5][6] The many shortcomings of platinum drugs have stimulated the interest of scientific researchers in finding other low-toxicity and low-side-effect metal drugs that can replace platinum drugs. [7][8][9][10][11] At present, different types of metal complexes represented by ruthenium, iridium, nickel, rhodium, iron, and copper have shown excellent antitumor ability with a unique antitumor mechanism.…”

Section: Introductionmentioning

confidence: 99%

In vitro and in vivo antitumor activity of novel half-sandwich ruthenium complexes containing quinoline derivative ligands

Kandawa‐Schulz

Shao

et al. 2023

Dalton Trans.

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Platinum complexes as inhibitors of DNA repair protein Ku70 and topoisomerase IIα in cancer cells

Cited by 4 publications

References 50 publications

Understanding Cancer’s Defense against Topoisomerase-Active Drugs: A Comprehensive Review

Understanding Cancer’s Defense against Topoisomerase-Active Drugs: A Comprehensive Review

Cracking the Code: Understanding Cancer’s Defense against Topoisomerase-Active Drugs: A Comprehensive Review

In vitro and in vivo antitumor activity of novel half-sandwich ruthenium complexes containing quinoline derivative ligands

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