NF-κB modulation and ionizing radiation: mechanisms and future directions for cancer treatment

Magné, Nicolas; Toillon, Robert‐Alain; Bottero, Virginie; Didelot, Céline; Houtte, Paul Van; Gérard, Jean-Pierre; Peyron, Jean‐François

doi:10.1016/j.canlet.2005.01.022

Cited by 170 publications

(127 citation statements)

References 94 publications

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“…Upregulation of miR-100 therefore sensitized cells to radiation (55). In addition to involvement in numerous important processes such as immune and inflammatory response, the transcription factor NF-jB is also known as crucial early response gene responsible for modulating cellular response and apoptosis in response to injury (68). Interestingly, the activated NF-jB pathway is linked to radioresistance, and suppression of this pathway might offer another opportunity to overcome radioresistance (69).…”

Section: Mirnas Regulating Relevant Cellular Signaling Pathwaysmentioning

confidence: 99%

MicroRNAs and Their Impact on Radiotherapy for Cancer

et al. 2016

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Section: Mirnas Regulating Relevant Cellular Signaling Pathwaysmentioning

confidence: 99%

MicroRNAs and Their Impact on Radiotherapy for Cancer

et al. 2016

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“…Decrease in HSP70 by the combination of these two treatments compared to RT alone suggests a radiosensitizer effect of DHA, because high expression of HSP70 can lead to radioresistance. 23 ROS consequently mediate activation of NF-kB, 24 whose high constitutive expression is important to maintain cell viability in cancer cells. 25 NF-kB is also the most important mediator in radioresistance.…”

Section: Early Apoptosis (%)mentioning

confidence: 99%

“…28 Therefore, NFkB probably has a primordial effect in maintaining cell apoptosis induced by inflammatory challenge and at the same time modulating release of factors that are involved in cell survival. 24 Modulation of NF-kB consequently led to change in expression of COX-2, a down-stream inflammatory protein that plays an essential role in CRC carcinogenesis and treatment. 29 u-3 PUFAs could inhibit CRC cell proliferation with a decrease in proinflammatory proteins, including iNOS and COX-2.…”

Section: Early Apoptosis (%)mentioning

confidence: 99%

Interaction of ω-3 polyunsaturated fatty acids with radiation therapy in two different colorectal cancer cell lines

et al. 2014

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Methods: LS174T and HT-29 cells were treated with 20 or 50 mmol/L EPA or DHA followed by single X-ray RT of 0, 2 or 4 Gy, to evaluate cell survival, apoptosis, peroxide and malondialdehyde productions. Inflammation-and apoptosis-related proteins were analyzed by Western Blot. ANOVAs were used for statistical analysis. Results: LS174T was more sensitive to RT than HT-29. DHA and to a lesser extent EPA increased cell death, apoptosis and peroxide production after RT in LS174T and to a lesser extent in HT-29 (p < 0.05). This was associated with increased expression of heat shock protein 70, decreased expression of NF-kB p65, COX-2 and Bcl-2 proteins. Conclusions: The effect of RT combination with DHA and to a lesser extent EPA was synergistic in the radio-sensitive LS174T cells, but additive in the radio-resistant HT-29 cells. This enhanced cytotoxicity was provoked at least partly by lipid peroxidation, which consequently modulated inflammatory response and induced apoptosis.

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“…100 U ml ¡1 TNF-was added 6 or 18 h after irradiation/sham irradiation. Gels are representative of three independent experiments from three diVerent isolations; ExCO 100-fold excess cold NF B oligonucleotide; -AB EMSA without NF B p65 supershift antibody Discussion NF B is an essential component of ionizing radiation-triggered signal transduction pathways that can lead either to cell death or survival, depending on the respective cell type (for a review see [17]), and numerous studies have demonstrated that inhibition of NF B by diVerent means increased sensitivity of cancer cells to the apoptotic action of diverse eVectors such as TNF-, chemo-or radiotherapies (for review see [18]). In both primary rat hepatocytes and a non-transformed rat hepatocyte cell line, inhibition of NF B-activity by adenoviral delivery of a I B superrepressor sensitized these cells to death from TNF- [19,20].…”

Section: Evect Of I B-antisense On Susceptibility Of Irradiated Hepatmentioning

confidence: 99%

Irradiation leads to sensitization of hepatocytes to TNF-α-mediated apoptosis by upregulation of IκB expression

Gürleyen

Christiansen

Tello

et al. 2008

Radiat Environ Biophys

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This study aimed to reveal the pathophysiological signalling responsible for radiation-induced sensitization of hepatocytes to TNF--mediated apoptosis. I B was upregulated in irradiated hepatocytes. Administration of I B antisense oligonucleotides prior to irradiation inhibited occurrence of apoptosis after TNF-administration. Caspases-8, -9 and -3 activities were increased in irradiated hepatocytes and downregulation of apoptosis by I B antisense oligonucleotides was mediated by suppression of caspases-9 and -3 activation but not of caspase-8 activation, suggesting that radiation-induced sensitization of hepatocytes to TNF--mediated apoptosis additionally requires changes upstream of caspase-8 activation. Herein, upregulation of FLIP may play a crucial role. Cleavage of bid, upregulation of bax, downregulation of bcl-2 and release of cytochrome c after TNF--administration depend on radiation-induced upregulation of I B, thus demonstrating an apoptosis permitting eVect of I B.

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NF-κB modulation and ionizing radiation: mechanisms and future directions for cancer treatment

Cited by 170 publications

References 94 publications

MicroRNAs and Their Impact on Radiotherapy for Cancer

MicroRNAs and Their Impact on Radiotherapy for Cancer

Interaction of ω-3 polyunsaturated fatty acids with radiation therapy in two different colorectal cancer cell lines

Irradiation leads to sensitization of hepatocytes to TNF-α-mediated apoptosis by upregulation of IκB expression

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