Results 31 to 40 of about 24,752 (187)

Loss of IGF‐1R impairs DNA‐PKcs recruitment to chromatin leading to defective end‐joining

Molecular Oncology, EarlyView.
IGF‐1R promotes radioresistance by facilitating DNA‐PKcs recruitment to chromatin, enabling non‐homologous end‐joining (NHEJ) repair of double‐strand breaks. Inhibition or loss of IGF‐1R disrupts this recruitment to damage sites, driving compensatory reliance on microhomology‐mediated end‐joining (MMEJ) repair.
Matthew O. Ellis, Jack V. Mills, Wojciech Niedzwiedz, Valentine M. Macaulay   +3 more
wiley   +1 more source

Nuclear pore links Fob1‐dependent rDNA damage relocation to lifespan control

FEBS Open Bio, EarlyView.
Damaged rDNA accumulates at a specific perinuclear interface that couples nucleolar escape with nuclear envelope association. Nuclear pores at this site help inhibit Fob1‐induced rDNA instability. This spatial organization of damage handling supports a functional link between nuclear architecture, rDNA stability, and replicative lifespan in yeast.
Yamato Okada, Mina Iwaki, Kyosuke Hagiri, Rei Izumi, Masahiko Harata, Chihiro Horigome   +5 more
wiley   +1 more source

Implications of DNA damage response and immunotherapy in tumor therapy

Cell Communication and Signaling
Tumorigenesis is closely related to defects in DNA damage response (DDR), which plays an important role in maintaining genomic integrity. The DDR process includes DNA damage recognition, cell cycle checkpoint pathway activation, and DNA damage repair. On
Wenqing Li, Binghang Li, Chang Cai, Jie Chen, Yiqiu Li, Rongrui Liang, Jing Zhao   +6 more
doaj   +1 more source

PARP inhibitors induce a senescence phenotype in non‐small cell lung carcinoma cell lines

FEBS Open Bio, EarlyView.
Talazoparib is the most potent inducer of senescence among different PARP1 inhibitors in human NSCLC cells. In the absence of PARP, no senescence phenotype was observed, demonstrating that PARP1 is necessary for the induction of senescence by this inhibitor.
Camille Huart, Manon Van den Abbeel, Christoph Schifflers, Karim Bouhjar, Andrea Scarmelotto, Alexis Khelfi, Anne‐Catherine Wera, Carine Michiels   +7 more
wiley   +1 more source

The RNA Processing Factor Y14 Participates in DNA Damage Response and Repair

iScience, 2019
Summary: DNA repair deficiency leads to genome instability and hence human disease. Depletion of the RNA processing factor Y14/RBM8A in cultured cells or Rbm8a haplodeficiency in the developing mouse cortex results in the accumulation of DNA damage.
Tzu-Wei Chuang, Chia-Chen Lu, Chun-Hao Su, Pei-Yu Wu, Sarasvathi Easwvaran, Chi-Chieh Lee, Hung-Che Kuo, Kuan-Yang Hung, Kuo-Ming Lee, Ching-Yen Tsai, Woan-Yuh Tarn   +10 more
doaj   +1 more source

Blood‐based proteomic profiling reveals context‐dependent changes in BCL2‐associated signaling during taxane therapy in breast cancer patients

FEBS Open Bio, EarlyView.
Chemotherapy side effects significantly impact cancer survivors' quality of life. Using protein levels in blood samples from breast cancer patients before and after 12 weeks of taxane treatment, we detected treatment‐dependent changes in calcium signaling and aging pathways associated with cancer recurrence.
Saira Munshani, Eiman Y. Ibrahim, Rozalyn L. Rodwin, Leah M. Ferrucci, Kim Blenman, Maryam Lustberg, Barbara E. Ehrlich   +6 more
wiley   +1 more source

Genotoxin-producing Salmonella enterica induces tissue-specific types of DNA damage and DNA damage response outcomes

Frontiers in Immunology
IntroductionTyphoid toxin-expressing Salmonella enterica causes DNA damage in the intestinal mucosa in vivo, activating the DNA damage response (DDR) in the absence of inflammation.
Maria Lopez Chiloeches, Anna Bergonzini, Océane C. B. Martin, Nicole Bergstein, Saskia F. Erttmann, Saskia F. Erttmann, Kyaw Min Aung, Nelson O. Gekara, Nelson O. Gekara, Javier F. Avila Cariño, Ioannis S. Pateras, Teresa Frisan   +11 more
doaj   +1 more source

A p53-independent role for the MDM2 antagonist Nutlin-3 in DNA damage response initiation

BMC Cancer, 2011
Background The mammalian DNA-damage response (DDR) has evolved to protect genome stability and maximize cell survival following DNA-damage. One of the key regulators of the DDR is p53, itself tightly regulated by MDM2. Following double-strand DNA breaks (
Kumar Sonia, Valentine Jane M, Moumen Abdeladim   +2 more
doaj   +1 more source

Chromosomal Instability Drives Glioblastoma Heterogeneity and Therapeutic Opportunities

Advanced Science, EarlyView.
ABSTRACT Glioblastoma, the most aggressive and lethal form of brain cancer, is defined by profound genomic instability, with Chromosomal Instability (CIN) playing a central role in driving tumor progression, therapy resistance, and poor prognosis. CIN is characterized by numerical and structural alterations, is driven by mechanisms such as mitotic ...
Amarnath Pal, Milan Patra, Rianita Mondal, Shubhasis Haldar   +3 more
wiley   +1 more source

Inhibition of SIRT7 Overcomes Radioresistance in Pancreatic Neuroendocrine Tumors by Reactivating MEN1 Expression

Advanced Science, EarlyView.
Pancreatic neuroendocrine tumors frequently silence MEN1 through epigenetic mechanisms. Here, SIRT7 recruits DNMT1 to the MEN1 promoter, drives hypermethylation, and enhances DNA repair. Inhibiting SIRT7 restores MEN1, reduces MRN complex abundance, impairs double‐strand break repair, and sensitizes PanNET models to radiation, supporting SIRT7 as a ...
Jianyun Jiang, Yan Wang, Yi Qin, Luohai Chen, Xiaowu Xu, Guixiong Fan, Desheng Jing, Miaoyan Wei, Xianjun Yu, Junfeng Xu, Shunrong Ji, Jie Chen   +11 more
wiley   +1 more source