Radiation-Induced Cell Death: Signaling and Pharmacological Modulation

2018 ◽  
Vol 23 (1-2) ◽  
pp. 13-37 ◽  
Author(s):  
Alex Philchenkov
Keyword(s):  
Cell Death ◽  
Pharmacological Modulation ◽  
Radiation Induced ◽  
Cell Death Signaling

scholarly journals The radiation-induced cell-death signaling pathway is activated by concurrent use of cisplatin in sequential biopsy specimens from patients with cervical cancer

2007 ◽  
Vol 6 (6) ◽  
pp. 905-911 ◽  
Author(s):  
Mayumi Iwakawa ◽  
Tatsuya Ohno ◽  
Kaori Imadome ◽  
Miyako Nakawatari ◽  
Ken-Ichi Ishikawa ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cell Death ◽  
Signaling Pathway ◽  
Biopsy Specimens ◽  
Concurrent Use ◽  
Radiation Induced ◽  
Cell Death Signaling

Role of WWOX WOX1 in Alzheimer s disease pathology and in cell death signaling

10.2741/s358 ◽  
2013 ◽  
Vol S5 (1) ◽  
pp. 72-85 ◽  
Author(s):  
Chih-Chung Teng
Keyword(s):  
Cell Death ◽  
Cell Death Signaling

scholarly journals A radiosensitizer, gallotannin-rich extract from Bouea macrophylla seeds, inhibits radiation-induced epithelial-mesenchymal transition in breast cancer cells

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jiraporn Kantapan ◽  
Siwaphon Paksee ◽  
Aphidet Duangya ◽  
Padchanee Sangthong ◽  
Sittiruk Roytrakul ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Dna Damage ◽  
Cell Death ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Breast Cancer Cell Lines ◽  
Mesenchymal Transition ◽  
Mammosphere Formation ◽  
Radiation Induced

Abstract Background Radioresistance can pose a significant obstacle to the effective treatment of breast cancers. Epithelial–mesenchymal transition (EMT) is a critical step in the acquisition of stem cell traits and radioresistance. Here, we investigated whether Maprang seed extract (MPSE), a gallotannin-rich extract of seed from Bouea macrophylla Griffith, could inhibit the radiation-induced EMT process and enhance the radiosensitivity of breast cancer cells. Methods Breast cancer cells were pre-treated with MPSE before irradiation (IR), the radiosensitizing activity of MPSE was assessed using the colony formation assay. Radiation-induced EMT and stemness phenotype were identified using breast cancer stem cells (CSCs) marker (CD24−/low/CD44+) and mammosphere formation assay. Cell motility was determined via the wound healing assay and transwell migration. Radiation-induced cell death was assessed via the apoptosis assay and SA-β-galactosidase staining for cellular senescence. CSCs- and EMT-related genes were confirmed by real-time PCR (qPCR) and Western blotting. Results Pre-treated with MPSE before irradiation could reduce the clonogenic activity and enhance radiosensitivity of breast cancer cell lines with sensitization enhancement ratios (SERs) of 2.33 and 1.35 for MCF7 and MDA-MB231cells, respectively. Pretreatment of breast cancer cells followed by IR resulted in an increased level of DNA damage maker (γ-H2A histone family member) and enhanced radiation-induced cell death. Irradiation induced EMT process, which displayed a significant EMT phenotype with a down-regulated epithelial marker E-cadherin and up-regulated mesenchymal marker vimentin in comparison with untreated breast cancer cells. Notably, we observed that pretreatment with MPSE attenuated the radiation-induced EMT process and decrease some stemness-like properties characterized by mammosphere formation and the CSC marker. Furthermore, pretreatment with MPSE attenuated the radiation-induced activation of the pro-survival pathway by decrease the expression of phosphorylation of ERK and AKT and sensitized breast cancer cells to radiation. Conclusion MPSE enhanced the radiosensitivity of breast cancer cells by enhancing IR-induced DNA damage and cell death, and attenuating the IR-induced EMT process and stemness phenotype via targeting survival pathways PI3K/AKT and MAPK in irradiated breast cancer cells. Our findings describe a novel strategy for increasing the efficacy of radiotherapy for breast cancer patients using a safer and low-cost natural product, MPSE.

scholarly journals Changes in Plant Mitochondrial Electron Transport Alter Cellular Levels of Reactive Oxygen Species and Susceptibility to Cell Death Signaling Molecules

2006 ◽  
Vol 47 (11) ◽  
pp. 1509-1519 ◽  
Author(s):  
Sasan Amirsadeghi ◽  
Christine A. Robson ◽  
Allison E. McDonald ◽  
Greg C. Vanlerberghe
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Electron Transport ◽  
Reactive Oxygen ◽  
Signaling Molecules ◽  
Oxygen Species ◽  
Cell Death Signaling

scholarly journals PKCε-mediated ERK1/2 activation involved in radiation-induced cell death in NIH3T3 cells

2003 ◽  
Vol 1593 (2-3) ◽  
pp. 219-229 ◽  
Author(s):  
Yoon-Jin Lee ◽  
Jae-Won Soh ◽  
Doo-Il Jeoung ◽  
Chul-Koo Cho ◽  
Gil Ja Jhon ◽  
...  
Keyword(s):  
Cell Death ◽  
Nih3t3 Cells ◽  
Radiation Induced

scholarly journals Cell Death Related Proteins Beyond Apoptosis in the CNS

2022 ◽  
Vol 9 ◽  
Author(s):  
Bazhena Bahatyrevich-Kharitonik ◽  
Rafael Medina-Guzman ◽  
Alicia Flores-Cortes ◽  
Marta García-Cruzado ◽  
Edel Kavanagh ◽  
...  
Keyword(s):  
Cell Death ◽  
Protein Function ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Original Function ◽  
New Concepts ◽  
Cytoskeleton Reorganization ◽  
Caspase Substrates ◽  
Cell Death Signaling ◽  
Related Proteins

Cell death related (CDR) proteins are a diverse group of proteins whose original function was ascribed to apoptotic cell death signaling. Recently, descriptions of non-apoptotic functions for CDR proteins have increased. In this minireview, we comment on recent studies of CDR proteins outside the field of apoptosis in the CNS, encompassing areas such as the inflammasome and non-apoptotic cell death, cytoskeleton reorganization, synaptic plasticity, mitophagy, neurodegeneration and calcium signaling among others. Furthermore, we discuss the evolution of proteomic techniques used to predict caspase substrates that could potentially explain their non-apoptotic roles. Finally, we address new concepts in the field of non-apoptotic functions of CDR proteins that require further research such the effect of sexual dimorphism on non-apoptotic CDR protein function and the emergence of zymogen-specific caspase functions.

scholarly journals A FORMULA TO PREDICT THE TRANSMISSION FREQUENCY OF ACENTRIC FRAGMENTS

Genetics ◽  
1972 ◽  
Vol 72 (4) ◽  
pp. 777-782
Author(s):  
A V Carrano
Keyword(s):  
Cell Death ◽  
Poisson Distribution ◽  
Transmission Frequency ◽  
Chromosomal Deletions ◽  
Radiation Induced ◽  
Fragment Distribution ◽  
The Mean ◽  
Th 1

ABSTRACT A formula, based on the Poisson distribution of radiation-induced chromosomal deletions, was derived to predict the frequency of transmission of acentric fragments between subsequent mitoses. The frequency of deletions observed in the i  th + 1 division subsequent to fragment distribution at the i  th division anaphase is independent of the cell death resulting from fragment loss. Further, the transmission frequency of chromosome acentric fragments is mathematically equal to the fragment frequency observed in the i  th + 1 generation divided by the mean fragment frequency in the i  th generation. The formula was also extended to chromatid deletions.

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