Acta Scientific Gastrointestinal Disorders (ASGIS)(ISSN: 2582-1091)

Research Article Volume 5 Issue 3

ATR Mediated Activity of Molecular Editors on Oncological Cells

Miss Akanksha Singh*

Dr Ambedkar College, Deeksha Bhoomi, Nagpur, Maharashtra, India

*Corresponding Author: Miss Akanksha Singh, Dr Ambedkar College, Deeksha Bhoomi, Nagpur, Maharashtra, India.

Received: December 14, 2021; Published: February 25, 2022


CRISPR Cas 9, a biologist editing guide has conquered molecular genetics with its supreme ability to edit the human genome thus eradicating the complexity involved in proteomics and recombinant DNA technology to cure many genetic diseases. In this study, the CRISPR Cas 9 machinery has been applied to demonstrate anti tumoral activity with the aid of molecular sensors working in the DNA replication like ATR that, at times of normal replication allows the stalled replication forks to move further that will eliminate circumstances leading to apoptosis. This biomolecule is used as anti- cancer tool to prevent detrimental effects of malignancies associated with the cancer. During the progression S-phase, most of the times, the cell accurately completes the replication but when cell senses the mutation or any physical damage in its way of replicating DNA, the replication machinery gets halted thus accumulating many ssDNA molecules and this stimulates ATR molecule to bind and pave the way for completion of replication. This review juxtaposed the anticancer effects in mammalian and mouse cells and indicated ATR to be important molecule in diagnosis of cancer.

Keywords: CRISPR Cas 9; Proteomics; Molecular Sensors; ATR; Apoptosis; Malignancies


  1. Lino CA., et al. “Delivering CRISPR: a review of the challenges and approaches”. Drug Delivery25.1 (2018): 1234-1257.
  2. Cui YR., et al. “Allosteric inhibition of CRISPR-Cas9 by bacteriophage-derived peptides”. Genome Biology1 (2020): 51.
  3. Jiang F and Doudna JA. “CRISPR-Cas9 Structures and Mechanisms”. Annual Review of Biophysics 46 (2017): 505-529.
  4. Ruiz S., et al. “A Genome-wide CRISPR Screen Identifies CDC25A as a Determinant of Sensitivity to ATR Inhibitors”. Molecular Cell2 (2016): 307-313.
  5. Zou L. “Single- and double-stranded DNA: building a trigger of ATR-mediated DNA damage response”. Genes and Development8 (2007): 879-885.
  6. Bass TE., et al. “ETAA1 acts at stalled replication forks to maintain genome integrity”. Nature Cell Biology 11 (2016): 1185-1195.
  7. Haahr P., et al. “Activation of the ATR kinase by the RPA-binding protein ETAA1”. Nature Cell Biology11 (2016): 1196-1207.
  8. Delacroix S., et al. “The Rad9-Hus1-Rad1 (9-1-1) clamp activates checkpoint signalling via TopBP1”. Genes and Development 12 (2007): 1472-1477.
  9. Bermudez VP., et al. “Loading of the human 9-1-1 checkpoint complex onto DNA by the checkpoint clamp loader hRad17-replication factor C complex in vitro”. Proceedings of the National Academy of Sciences of the United States of America4 (2003): 1633-1638.
  10. Kumagai A and Dunphy WG. “Claspin, a novel protein required for the activation of Chk1 during a DNA replication checkpoint response in Xenopus egg extracts”. Molecular Cell6.4 (2000): 839-849.
  11. Mailand N., et al. “Rapid destruction of human Cdc25A in response to DNA damage”. Science 5470 (2000): 1425-1429.
  12. Yekezare M., et al. “Controlling DNA replication origins in response to DNA damage - inhibit globally, activate locally”. Journal of Cell Science Pt 6 (2013): 1297-1306.
  13. Hart T., et al. “High-Resolution CRISPR Screens Reveal Fitness Genes and Genotype-Specific Cancer Liabilities”. Cell 163.6 (2015): 1515-1526.
  14. Wang T., et al. “Genetic screens in human cells using the CRISPR-Cas9 system”. Science343.6166 (2014): 80-84.
  15. MCF 10A Cell Line. (n.d.) (2020).
  16. Ramlee MK., et al. “High-throughput genotyping of CRISPR/Cas9-mediated mutants using fluorescent PCR-capillary gel electrophoresis”. Scientific Reports5 (2015): 15587.
  17. Hustedt N., et al. “A consensus set of genetic vulnerabilities to ATR inhibition”. Open Biology 9.9 (2019): 190156.
  18. Hall AB., et al. “Potentiation of tumor responses to DNA damaging therapy by the selective ATR inhibitor VX-970”. Oncotarget, 14 (2014): 5674-5685.
  19. Rundle S., et al. “Targeting the ATR-CHK1 Axis in Cancer Therapy”. Cancers5 (2017).
  20. Schoppy DW and Brown EJ. “Chk’ing p53-deficient breast cancers”. The Journal of Clinical Investigation122.4 (2012): 1202-1205.
  21. Williams JS., et al. “The role of RNase H2 in processing ribonucleotides incorporated during DNA replication”. DNA Repair53 (2017): 52-58.
  22. Shen T and Huang S. “The role of Cdc25A in the regulation of cell proliferation and apoptosis”. Anti-Cancer Agents in Medicinal Chemistry 12.6 (2012): 631-639.


Citation: Miss Akanksha Singh. “ATR Mediated Activity of Molecular Editors on Oncological Cells". Acta Scientific Gastrointestinal Disorders 5.3 (2022): 59-64.


Copyright: © 2022 Miss Akanksha Singh. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


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