Typical cell signaling response to ionizing radiation: DNA damage and extranuclear damage

Yu, Hui

doi:10.1007/s11670-012-0083-1

Cited by 27 publications

(21 citation statements)

References 77 publications

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“…The cytotoxicity caused by ionizing radiation is mainly the result of DNA damage. Radiation induces several forms of DNA damage, which include SSBs, DSBs, sugar and base modifications and DNA-protein crosslinks ( 95 , 96 ). Among these, DSBs are not only a dominant form of damage caused by ionizing radiation ( 97 , 98 ), but also is the most deadly form of DNA damage, as unrepaired DSBs can lead to lethality of cells ( 97 , 99 ).…”

Section: Dna Repair Pathwaysmentioning

confidence: 99%

Radiation-induced signaling pathways that promote cancer cell survival (Review)

Hein

Ouellette

Yan

2014

International Journal of Oncology

149

122

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Radiation therapy is a staple cancer treatment approach that has significantly improved local disease control and the overall survival of cancer patients. However, its efficacy is still limited by the development of radiation resistance and the presence of residual disease after therapy that leads to cancer recurrence. Radiation impedes cancer cell growth by inducing cytotoxicity, mainly caused by DNA damage. However, radiation can also simultaneously induce multiple pro-survival signaling pathways, such as those mediated by AKT, ERK and ATM/ATR, which can lead to suppression of apoptosis, induction of cell cycle arrest and/or initiation of DNA repair. These signaling pathways act conjointly to reduce the magnitude of radiation-induced cytotoxicity and promote the development of radioresistance in cancer cells. Thus, targeting these pro-survival pathways has great potential for the radiosensitization of cancer cells. In the present review, we summarize the current literature on how these radiation-activated signaling pathways promote cancer cell survival.

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Section: Dna Repair Pathwaysmentioning

confidence: 99%

Radiation-induced signaling pathways that promote cancer cell survival (Review)

Hein

Ouellette

Yan

2014

International Journal of Oncology

149

122

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“…Furthermore, there are now some studies that have reported the induction of biological effects in cells that have not been directly irradiated and where no direct traversal of a charged particle has occurred [221,222]. These effects are referred to as bystander effects and, although their exact mechanisms are yet to be elucidated, there is evidence across a number of studies, with disparate methodologies, for cellular signalling [155,223–226]. Moreover, many bystander effects have been reported at low doses and a response that augments the effects of exposure across large numbers of cells could be a major contributor to the effects observed at low doses.…”

Section: Implications At Low Dosesmentioning

confidence: 99%

The Cellular and Molecular Carcinogenic Effects of Radon Exposure: A Review

Robertson

Allen

Laney

et al. 2013

IJMS

116

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Radon-222 is a naturally occurring radioactive gas that is responsible for approximately half of the human annual background radiation exposure globally. Chronic exposure to radon and its decay products is estimated to be the second leading cause of lung cancer behind smoking, and links to other forms of neoplasms have been postulated. Ionizing radiation emitted during the radioactive decay of radon and its progeny can induce a variety of cytogenetic effects that can be biologically damaging and result in an increased risk of carcinogenesis. Suggested effects produced as a result of alpha particle exposure from radon include mutations, chromosome aberrations, generation of reactive oxygen species, modification of the cell cycle, up or down regulation of cytokines and the increased production of proteins associated with cell-cycle regulation and carcinogenesis. A number of potential biomarkers of exposure, including translocations at codon 249 of TP53 in addition to HPRT mutations, have been suggested although, in conclusion, the evidence for such hotspots is insufficient. There is also substantial evidence of bystander effects, which may provide complications when calculating risk estimates as a result of exposure, particularly at low doses where cellular responses often appear to deviate from the linear, no-threshold hypothesis. At low doses, effects may also be dependent on cellular conditions as opposed to dose. The cellular and molecular carcinogenic effects of radon exposure have been observed to be both numerous and complex and the elevated chronic exposure of man may therefore pose a significant public health risk that may extend beyond the association with lung carcinogenesis.

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“…In addition, environmental pollutants may influence the intracellular signaling machinery that mediates the regulation of gene expression. For example, ionizing radiation is capable of causing the formation of reactive oxygen species which damage various proteins including regulatory ones [ 16 ]. Formaldehyde promotes formation of protein-protein and DNA-protein crosslinks [ 17 ].…”

Section: Introductionmentioning

confidence: 99%

Exhaustive data mining comparison of the effects of low doses of ionizing radiation, formaldehyde and dioxins

et al. 2014

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BackgroundIonizing radiation in low doses is the ubiquitous environmental factor with harmful stochastic effects. Formaldehyde is one of the most reactive household and industrial pollutants. Dioxins are persistent organic pollutants and most potent synthetic poisons effective even at trace concentrations. Environmental pollutants are capable of altering the expression of a variety of genes. To identify the similarities and differences in the effects of low-dose ionizing radiation, formaldehyde and dioxin on gene expression, we performed the bioinformatic analysis of all available published data.ResultsWe found that that in addition to the common p53-, ATM- and MAPK-signaling stress response pathways, genes of cell cycle regulation and proinflammatory cytokines, the studied pollutants induce a variety of other molecular processes.ConclusionsThe observed patterns provide new insights into the mechanisms of the adverse effects associated with these pollutants. They can also be useful in the development of new bio-sensing methods for detection of pollutants in the environment and combating the deleterious effects.

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Typical cell signaling response to ionizing radiation: DNA damage and extranuclear damage

Cited by 27 publications

References 77 publications

Radiation-induced signaling pathways that promote cancer cell survival (Review)

Radiation-induced signaling pathways that promote cancer cell survival (Review)

The Cellular and Molecular Carcinogenic Effects of Radon Exposure: A Review

Exhaustive data mining comparison of the effects of low doses of ionizing radiation, formaldehyde and dioxins

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