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Volume 63, Issue 5, 19 June 2015, Pages 357-366
a
Laboratory for Translational Oncology and Personalized Medicine, Rashid Latif Medical College, Lahore, Pakistan
b Department of Medical Laboratory Science and Biotechnology, Kaohsiung Medical University, Kaohsiung, Taiwan
c Doctor Degree Program in Marine Biotechnology, National Sun Yat-sen University/Academia Sinica, Kaohsiung, Taiwan
b Department of Medical Laboratory Science and Biotechnology, Kaohsiung Medical University, Kaohsiung, Taiwan
c Doctor Degree Program in Marine Biotechnology, National Sun Yat-sen University/Academia Sinica, Kaohsiung, Taiwan
Abstract
Double-stranded
breaks (DSBs) are cytotoxic DNA lesions caused by oxygen radicals,
ionizing radiation, and radiomimetic chemicals. Increasing understanding
of DNA damage signaling has provided an ever-expanding list of
modulators reported to orchestrate DNA damage repair and ataxia
telangiectasia mutated (ATM) is the master regulator and main transducer
of the DSB response. Increasingly, it is being realized that DNA damage
response is a synchronized and branched network that functionalizes
different molecular cascades to activate special checkpoints, thus
temporarily arresting progression of the cell cycle while damage is
being assessed and processed. It is noteworthy that both nutrigenetics
and nutrigenomics have revolutionized the field of molecular biology and
rapidly accumulating experimental evidence has started to shed light on
biological activities of a wide range of phytochemicals reported to
modulate cell cycle, DNA repair, cell growth, differentiation and
apoptosis as evidenced by cell-based studies. In this review, we have
attempted to provide an overview of DNA damage signaling, how ATM
signaling regulates tumor necrosis factors-related apoptosis inducing
ligand (TRAIL)-induced intracellular network. We also illuminate on how
resveratrol, epigallocatechin gallate, curcumin, jaceosidin,
cucurbitacin, apigenin, genistein, and others trigger activation of ATM
in different cancer cells as well as agents for ATM inactivation.
Understanding the interplay of TRAIL-induced intracellular signaling and
ATM modulation of downstream effectors is very important. This holds
particularly for a reconceptualization of the apparently paradoxical
roles and therapeutically targetable for enhancing the response to DNA
damage-inducing therapy. © 2015, L. Hirszfeld Institute of Immunology
and Experimental Therapy, Wroclaw, Poland.
Author keywords
ATM inducers; ATM inhibitors; p53; Phytochemicals
Indexed keywords
EMTREE drug terms: apigenin; Artemisia princeps
extract; ATM protein; cucurbitacin; Curcuma longa extract; curcumin;
DNA; epigallocatechin gallate; genistein; Glycyrrhiza uralensis extract;
jaceosidin; lignan; plant extract; plant medicinal product; Polygonum cuspidatum extract; resveratrol; tumor necrosis factor related apoptosis inducing ligand; unclassified drug
EMTREE medical terms: Aglaia; arousal; Artemisia;
Artemisia douglasiana; Artemisia princeps; cacao; cancer cell;
Cinnamomum; coffee; Curcuma longa; DNA damage; double stranded DNA
break; Emilia sonchifolia; Eucalyptus; fruit; Glycyrrhiza uralensis;
Gynostemma pentaphyllum; human; inhibition kinetics; intracellular
signaling; medicinal plant; modulation; Myristica malabarica; nonhuman; persimmon; plant leaf; Polygonum cuspidatum; Review; rhubarb; sleep; Taiwania cryptomerioides; tea; vegetable
Chemicals and CAS Registry Numbers: apigenin, 520-36-5;
curcumin, 458-37-7; DNA, 9007-49-2; epigallocatechin gallate, 989-51-5;
genistein, 446-72-0; resveratrol, 501-36-0
ISSN: 0004069X
CODEN: AITEASource Type: Journal
Original language: English
DOI: 10.1007/s00005-015-0346-xDocument Type: Review
Publisher: Birkhauser Verlag AG
Funding Details
Number; Acronym; Sponsor: 103-2320-B-037-008; MOST; Ministry of Science and Technology of the People's Republic of China
