Results 71 to 80 of about 24,752 (187)

Losartan Enhances Radiosensitivity by Reversing Immunosuppressive Tumor Microenvironment Induced by Radiotherapy in TNBC

Cancer Science, EarlyView.
Our study demonstrates that the angiotensin receptor blocker losartan enhances the efficacy of radiotherapy in triple‐negative breast cancer by reversing the immunosuppressive tumor microenvironment. Losartan reprograms tumor‐associated macrophages, inhibits myeloid‐derived suppressor cell function, and boosts CD8+ T‐cell activity.
Xu Wang, Cuiwei Liu, Zihan Xia, Ting Hu, Yuting Li, Dan Han, Yunjie Song, Yuxi Ma, Yanxia Zhao   +8 more
wiley   +1 more source

Posttranscriptional regulation of gene expression – adding another layer of complexity to the DNA damage response

Frontiers in Genetics, 2012
In response to DNA damage, cells activate a complex, kinase-based signaling network to arrest the cell cycle and allow time for DNA repair, or, if the extend of damage is beyond repair capacity, induce apoptosis.
Jorge eBoucas, Katja eHöpker, Shuhua eChen, Grit Sophie Herter-Sprie, Mladen eJokic, Arina eRiabinska, Hans Christian Reinhardt   +6 more
doaj   +1 more source

Targeting Cell Cycle Vulnerabilities in Cancers: Emerging Strategies for Therapeutic Development

Cancer Science, EarlyView.
Dysregulated cell cycle control often involves alternative compensatory pathways in cancers to maintain its robustness but provide unique targetable vulnerabilities. We overview recent insights on cancer‐specific vulnerabilities across the cell cycle and discuss how these can be used to develop new therapeutic strategies.
Nana Kamakura, Minji Jo, Motoko Takahashi, Toru Hirota   +3 more
wiley   +1 more source

CTCF/cohesin-binding sites are susceptible to replication-associated DNA damage and genomic instability in cancer cells

iScience
Summary: CTCF/cohesin-binding sites (CBSs) at the chromatin-loop anchors and topologically associating domains are frequently mutated in cancer; however, the underlying molecular mechanisms remain unclear. Here, we investigate whether CTCF and cohesin co-
Elangoli Ebrahimkutty Faseela, Dimple Notani, Radhakrishnan Sabarinathan   +2 more
doaj   +1 more source

NTAQ1 Promotes Hepatocellular Carcinoma Growth by Facilitating the Protein Degradation of the Tumor Suppressor PRDM2

Cancer Science, EarlyView.
Copy number variation analysis in The Cancer Genome Atlas identified NTAQ1 as a potential driver of HCC progression. NTAQ1 accelerates tumor growth by promoting the degradation of the tumor suppressor protein PRDM2, thereby impairing DNA repair and suppressing apoptosis. These findings indicate that NTAQ1 could be a valuable target for the treatment of
Tomohiko Ikehara, Hajime Otsu, Taro Tobo, Kiyotaka Hosoda, Tadashi Abe, Masahiro Hashimoto, Yusuke Nakano, Katsushi Dairaku, Yuya Ono, Yuki Miyata, Chihiro Matsumoto, Takanari Tatsumi, Satoshi Higuchi, Takashi Ofuchi, Akinori Tsujimoto, Yuki Ando, Qingjiang Hu, Yusuke Yonemura, Akira Shimizu, Takaaki Masuda, Yuji Soejima, Koshi Mimori   +21 more
wiley   +1 more source

Response to DNA damage: why do we need to focus on protein phosphatases?

Frontiers in Oncology, 2013
Eukaryotic cells are continuously threatened by unavoidable errors during normal DNA replication or various sources of genotoxic stresses that cause DNA damage or stalled replication.
Midori eShimada, Makoto eNakanishi
doaj   +1 more source

Oxidative Stress Drives Cell Cycle Stalling, Apoptosis and Metabolic Suppression in Cystatin B Deficient EPM1 Patient iPSCs

Cell Proliferation, EarlyView.
CSTB deficient EPM1 iPS cells manifest increased lysosomal activity and oxidative stress, which lead to DNA damage, cell cycle defects and increased apoptosis. As a protective response, metabolism is suppressed. Image created by BioRender https://BioRender.com/t44oc6h.
Shekhar Singh, Lidiia Plotnikova, Teemu Tiukuvaara, Reetta Kälviäinen, Riikka H. Hämäläinen   +4 more
wiley   +1 more source

DNA Damage Response (DDR) and DNA Repair. [PDF]

Int J Mol Sci, 2022
Vernì F.
europepmc   +1 more source

Cellular Morphometric Analysis (CellMorph)—a comprehensive imaging‐based tool for quantifying cellular phenotype heterogeneity and dynamics across biological processes

The FEBS Journal, EarlyView.
CellMorph is a groundbreaking tool that allows researchers to analyze multiple features from single cells, including cell size and shape, cytosolic staining and subcellular texture, nuclear staining, and morphometry. By evaluating images from both bright‐field and fluorescence microscopy, it also tracks changes in living cells during key processes such
Henrique Quaiato de Oliveira, Solon Andrades da Rosa, Luiza Cherobini Pereira, Laura Boose de Mendonça, Juliete Scholl, Fabrício Figueiró, Thais Cardoso Bitencourt, Davi Piovesan Echevarria, João Luiz Aldinucci Buzzo, Jessica Boschini D'Agostin, Danieli Rosane Dallemole, Carolina Oliveira, Fernanda Simas, Fernanda Saez‐Calazans, Débora Santos‐Sousa, Guido Lenz, Eduardo C. Filippi‐Chiela   +16 more
wiley   +1 more source

Proteostasis of organelles in aging and disease

The FEBS Journal, EarlyView.
Cells rely on regulated proteostasis mechanisms to keep their internal compartments functioning properly. When these mechanisms fail, damaged proteins accumulate, disrupting organelles, such as the nucleus, mitochondria, endoplasmic reticulum, Golgi, and lysosomes, as well as membraneless organelles, such as stress granules, processing bodies, the ...
Yara Nabawi, Cansu Doğan, Dunja Petrović, Gülce Perçin, Seda Koyuncu, David Vilchez   +5 more
wiley   +1 more source