2017
DOI: 10.18632/aging.101263
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Abstract: The DNA damage response enables cells to survive, maintain genome integrity, and to safeguard the transmission of high-fidelity genetic information. Upon sensing DNA damage, cells respond by activating this multifaceted DNA damage response leading to restoration of the cell, senescence, programmed cell death, or genomic instability if the cell survives without proper repair. However, unlike normal cells, cancer cells maintain a marked level of genomic instability. Because of this enhanced propensity to accumul… Show more

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Cited by 11 publications
(13 citation statements)
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References 85 publications
(113 reference statements)
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“…Our results are similar to those previously observed for the related DNA repair protein, RAD52, in lung cancer (8,9). RAD52 is predominantly recruited for DNA repair during the S phase of the cell cycle and plays a crucial role in the regulation of homologous recombination-related genomic instability in humans (25).…”
Section: Discussionsupporting
confidence: 91%
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“…Our results are similar to those previously observed for the related DNA repair protein, RAD52, in lung cancer (8,9). RAD52 is predominantly recruited for DNA repair during the S phase of the cell cycle and plays a crucial role in the regulation of homologous recombination-related genomic instability in humans (25).…”
Section: Discussionsupporting
confidence: 91%
“…In addition to drug resistance, proteins involved in DNA repair pathways have been implicated in tumor progression (22). For example, RAD52 has been linked to both the progression and risk of small cell lung cancer (SCLC) and NSCLC (8,9,23). In addition, RDM1 was previously shown to undergo stress-induced nucleolar accumulation, indicating it may function in the heat-shock response that is implicated in tumorigenesis (16).…”
Section: Discussionmentioning
confidence: 99%
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“…Defect in DDR related genes in tumor cells leads to impaired DNA repair, triggering apoptosis in tumor cells. Recent studies have demonstrated that DDR is important for the maintenance of tumor genome integrity, and dysregulation of DDR sensitizes tumor cells to chemotherapy [45][46][47][48]. Thus, inhibition of DDR pathway including HR and NHEJ via chemotherapeutic compounds selectively kill tumor cells that evolve to escape DDR and checkpoint signaling.…”
Section: Discussionmentioning
confidence: 99%
“…Unlike normal cells, cancer cells maintain a marked level of genomic instability and will be associated with replication stress factors such as cell cycle checkpoint loss, increased transcription, higher levels of metabolic stress, increased ROS formation and activation of oncogenic drivers . The principle hallmarks of cancers are their propensity to accumulate DNA damage and their decreased traditional repair capacity, leading cancer cells to become exceedingly more dependent on homologous recombination repair as a means of protection from the lethal effect of both spontaneous and therapy‐induced DSBs in DNA . Therefore, DNA‐damaging regimes, such as TB, could selectively induce tumour cell apoptosis by augmenting genomic instability, and the DNA repair mechanisms would work efficiently in normal cells in contrast to tumour cells.…”
Section: Discussionmentioning
confidence: 99%