Literature DB >> 29446719

DNA Double Strand Breaks Repair Inhibitors: Relevance as Potential New Anticancer Therapeutics.

Paulina Kopa1, Anna Macieja2, Grzegorz Galita2, Zbigniew J Witczak3, Tomasz Poplawski2.   

Abstract

DNA double-strand breaks are considered one of the most lethal forms of DNA damage. Many effective anticancer therapeutic approaches used chemical and physical methods to generate DNA double-strand breaks in the cancer cells. They include: IR and drugs which mimetic its action, topoisomerase poisons, some alkylating agents or drugs which affected DNA replication process. On the other hand, cancer cells are mostly characterized by highly effective systems of DNA damage repair. There are two main DNA repair pathways used to fix double-strand breaks: NHEJ and HRR. Their activity leads to a decreased effect of chemotherapy. Targeting directly or indirectly the DNA double-strand breaks response by inhibitors seems to be an exciting option for anticancer therapy and is a part of novel trends that arise after the clinical success of PARP inhibitors. These trends will provide great opportunities for the development of DNA repair inhibitors as new potential anticancer drugs. The main objective of this article is to address these new promising advances. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.

Entities:  

Keywords:  DNA double-strand breaks; Double-strand breaks repair; anti-cancer therapy; homologous recombination; inhibitors; non-homologouszzm321990end joining.

Mesh:

Substances:

Year:  2019        PMID: 29446719     DOI: 10.2174/0929867325666180214113154

Source DB:  PubMed          Journal:  Curr Med Chem        ISSN: 0929-8673            Impact factor:   4.530


  6 in total

1.  DNA double-strand breaks repair inhibitors potentiates the combined effect of VP-16 and CDDP in human colorectal adenocarcinoma (LoVo) cells.

Authors:  Paulina Kopa; Anna Macieja; Elzbieta Pastwa; Ireneusz Majsterek; Tomasz Poplawski
Journal:  Mol Biol Rep       Date:  2021-01-02       Impact factor: 2.316

2.  Hydroxygenkwanin Increases the Sensitivity of Liver Cancer Cells to Chemotherapy by Inhibiting DNA Damage Response in Mouse Xenograft Models.

Authors:  Chin-Chuan Chen; Chi-Yuan Chen; Shu-Fang Cheng; Tzong-Ming Shieh; Yann-Lii Leu; Wen-Yu Chuang; Kuang-Ting Liu; Shir-Hwa Ueng; Yin-Hwa Shih; Li-Fang Chou; Tong-Hong Wang
Journal:  Int J Mol Sci       Date:  2021-09-09       Impact factor: 6.208

3.  RAD51AP1 and RAD54L Can Underpin Two Distinct RAD51-Dependent Routes of DNA Damage Repair via Homologous Recombination.

Authors:  Platon Selemenakis; Neelam Sharma; Mollie E Uhrig; Jeffrey Katz; Youngho Kwon; Patrick Sung; Claudia Wiese
Journal:  Front Cell Dev Biol       Date:  2022-05-16

4.  Inhibition of DNA-PK potentiates the synergistic effect of NK314 and etoposide combination on human glioblastoma cells.

Authors:  Paulina Kopa; Anna Macieja; Izabela Gulbas; Elzbieta Pastwa; Tomasz Poplawski
Journal:  Mol Biol Rep       Date:  2019-10-03       Impact factor: 2.316

5.  Senescence Induction by Combined Ionizing Radiation and DNA Damage Response Inhibitors in Head and Neck Squamous Cell Carcinoma Cells.

Authors:  Clara Dobler; Tina Jost; Markus Hecht; Rainer Fietkau; Luitpold Distel
Journal:  Cells       Date:  2020-09-01       Impact factor: 6.600

Review 6.  Recent Advances in the Development of Non-PIKKs Targeting Small Molecule Inhibitors of DNA Double-Strand Break Repair.

Authors:  Jeremy M Kelm; Amirreza Samarbakhsh; Athira Pillai; Pamela S VanderVere-Carozza; Hariprasad Aruri; Deepti S Pandey; Katherine S Pawelczak; John J Turchi; Navnath S Gavande
Journal:  Front Oncol       Date:  2022-04-06       Impact factor: 5.738

  6 in total

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