scholarly journals Cell Cycle Checkpoint/DNA Repair Antagonist IC83

2020 ◽  
Author(s):  
Keyword(s):  
Cell Cycle ◽  
Dna Repair ◽  
Cell Cycle Checkpoint ◽  
Cycle Checkpoint

scholarly journals DNA repair and cell cycle checkpoint defects in a mouse model of ‘BRCAness’ are partially rescued by 53BP1 deletion

Cell Cycle ◽  
2018 ◽  
Vol 17 (7) ◽  
pp. 881-891 ◽  
Author(s):  
Sarah M. Misenko ◽  
Dharm S. Patel ◽  
Joonyoung Her ◽  
Samuel F. Bunting
Keyword(s):  
Cell Cycle ◽  
Dna Repair ◽  
Mouse Model ◽  
Cell Cycle Checkpoint ◽  
Cycle Checkpoint

scholarly journals ALDH1A1 Maintains Ovarian Cancer Stem Cell-Like Properties by Altered Regulation of Cell Cycle Checkpoint and DNA Repair Network Signaling

PLoS ONE ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. e107142 ◽  
Author(s):  
Erhong Meng ◽  
Aparna Mitra ◽  
Kaushlendra Tripathi ◽  
Michael A. Finan ◽  
Jennifer Scalici ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Dna Repair ◽  
Stem Cell ◽  
Cancer Stem Cell ◽  
Cell Cycle Checkpoint ◽  
Cycle Checkpoint ◽  
Altered Regulation ◽  
Regulation Of Cell Cycle

scholarly journals Inhibition of DNA Repair in Cancer Therapy: Toward a Multi-Target Approach

2020 ◽  
Vol 21 (18) ◽  
pp. 6684
Author(s):  
Samuele Lodovichi ◽  
Tiziana Cervelli ◽  
Achille Pellicioli ◽  
Alvaro Galli
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Dna Repair ◽  
Cancer Therapy ◽  
Clinical Outcome ◽  
Cancer Cells ◽  
Cell Cycle Checkpoint ◽  
Normal Cells ◽  
Cycle Checkpoint ◽  
Repair Pathways

Alterations in DNA repair pathways are one of the main drivers of cancer insurgence. Nevertheless, cancer cells are more susceptible to DNA damage than normal cells and they rely on specific functional repair pathways to survive. Thanks to advances in genome sequencing, we now have a better idea of which genes are mutated in specific cancers and this prompted the development of inhibitors targeting DNA repair players involved in pathways essential for cancer cells survival. Currently, the pivotal concept is that combining the inhibition of mechanisms on which cancer cells viability depends is the most promising way to treat tumorigenesis. Numerous inhibitors have been developed and for many of them, efficacy has been demonstrated either alone or in combination with chemo or radiotherapy. In this review, we will analyze the principal pathways involved in cell cycle checkpoint and DNA repair focusing on how their alterations could predispose to cancer, then we will explore the inhibitors developed or in development specifically targeting different proteins involved in each pathway, underscoring the rationale behind their usage and how their combination and/or exploitation as adjuvants to classic therapies could help in patients clinical outcome.

Spermidine/spermine N1-acetyltransferase overexpression in kidney epithelial cells disrupts polyamine homeostasis, leads to DNA damage, and causes G2 arrest

2007 ◽  
Vol 292 (3) ◽  
pp. C1204-C1215 ◽  
Author(s):  
Kamyar Zahedi ◽  
John J. Bissler ◽  
Zhaohui Wang ◽  
Anuradha Josyula ◽  
Lu Lu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Dna Damage ◽  
Dna Repair ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Dna Lesions ◽  
Cell Cycle Checkpoint ◽  
Cycle Checkpoint

Expression of spermidine/spermine N1-acetyltransferase (SSAT) increases in kidneys subjected to ischemia-reperfusion injury (IRI). Increased expression of SSAT in vitro leads to alterations in cellular polyamine content, depletion of cofactors and precursors of polyamine synthesis, and reduced cell proliferation. In our model system, a >28-fold increase in SSAT levels in HEK-293 cells leads to depletion of polyamines and elevation in the enzymatic activities of ornithine decarboxylase and S-adenosylmethionine decarboxylase, suggestive of a compensatory reaction to increased polyamine catabolism. Increased expression of SSAT also led to DNA damage and G2 arrest. The increased DNA damage was primarily due to the depletion of polyamines. Other factors such as increased production of H2O2 due to polyamine oxidase activity may play a secondary role in the induction of DNA lesions. In response to DNA damage the ATM/ATR → Chk1/2 DNA repair and cell cycle checkpoint pathways were activated, mediating the G2 arrest in SSAT-expressing cells. In addition, the activation of ERK1 and ERK2, which play integral roles in the G2/M transition, is impaired in cells expressing SSAT. These results indicate that the disruption of polyamine homeostasis due to enhanced SSAT activity leads to DNA damage and reduced cell proliferation via activation of DNA repair and cell cycle checkpoint and disruption of Raf → MEK → ERK pathways. We propose that in kidneys subjected to IRI, one mechanism through which increased expression of SSAT may cause cellular injury and organ damage is through induction of DNA damage and the disruption of cell cycle.

Sign in / Sign up

Export Citation Format

Share Document