Downregulation of eukaryotic initiation factor 4A1 improves radiosensitivity by delaying DNA double strand break repair in cervical cancer
نویسندگان
چکیده
منابع مشابه
Mechanisms of eukaryotic DNA double strand break repair.
For all cells, a DNA double strand break (DSB) is a dangerous lesion that can have profound consequences for the genome. If a DSB is encountered during mitosis, chromosomal separation may be adversely affected. Alternatively, during S phase a DSB may cause replication fork stalling or collapse. Improperly repaired DSBs can result in chromosomal rearrangements, senescence or activation of apopto...
متن کاملDNA Double-Strand Break Repair
ownloade C regulates a myriad of genes controlling cell proliferation, metabolism, differentiation, and apoptosis. lso controls the expression of DNA double-strand break (DSB) repair genes and therefore may be a ial target for anticancer therapy to sensitize cancer cells to DNA damage or prevent genetic instability. report, we studied whether MYC binds to DSB repair gene promoters and modulates...
متن کاملDNA double-strand break repair
The integrity of genomic DNA is crucial for its function. And yet, DNA in living cells is inherently unstable. It is subject to mechanical stress and to many types of chemical modification that may lead to breaks in one or both strands of the double helix. Within the cell, reactive oxygen species generated by normal respiratory metabolism can cause double-strand breaks, as can stalled DNA repli...
متن کاملRadiosensitization of cervical cancer cells via double-strand DNA break repair inhibition.
PURPOSE LY294002, a phosphatidylinositol 3-kinase (PI3K) inhibitor, has been found to radiosensitize various human cancer cells. However, its potential to act as an effective therapeutic agent is diminished by its toxicity levels. The purposes of this study were to determine the mechanism by which LY294002 radiosensitizes. MATERIALS AND METHODS Cell growth curves and clonogenic assays were pe...
متن کاملDouble strand break repair.
DNA double-strand breaks (DSBs) are the most dangerous form of DNA damage and can lead to death, mutation, or malignant transformation. Mammalian cells use three major pathways to repair DSBs: homologous recombination (HR), classical nonhomologous end joining (C-NHEJ), and alternative end joining (A-NHEJ). Cells choose among the pathways by interactions of the pathways with CtIP and 53BP1. HR i...
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ژورنال
عنوان ژورنال: Oncology Letters
سال: 2017
ISSN: 1792-1074,1792-1082
DOI: 10.3892/ol.2017.7040