Results 121 to 130 of about 234,206 (306)

Lysine-specific demethylase 1 (LSD1) suppresses cellular senescence by riboflavin uptake-dependent demethylation activity

Scientific Reports
Cellular senescence is defined as a permanent proliferation arrest caused by various stresses, including DNA damage. We have recently identified the riboflavin transporter SLC52A1, whose expression is increased in response to senescence-inducing stimuli.
Taiichi Osumi, Taiki Nagano, Tetsushi Iwasaki, Jotaro Nakanishi, Kazuyuki Miyazawa, Shinji Kamada   +5 more
doaj   +1 more source

SPOP E3 Ubiquitin Ligase Adaptor Promotes Cellular Senescence by Degrading the SENP7 deSUMOylase [PDF]

, 2015
Hengrui Zhu, Shancheng Ren, Benjamin G. Bitler, Katherine M. Aird, Zhigang Tu, Emmanuel Skordalakes, Yasheng Zhu, Jun Yan, Yinghao Sun, Rugang Zhang   +9 more
openalex   +1 more source

PYCR1 inhibition in bone marrow stromal cells enhances bortezomib sensitivity in multiple myeloma cells by altering their metabolism

Molecular Oncology, EarlyView.
This study investigated how PYCR1 inhibition in bone marrow stromal cells (BMSCs) indirectly affects multiple myeloma (MM) cell metabolism and viability. Culturing MM cells in conditioned medium from PYCR1‐silenced BMSCs impaired oxidative phosphorylation and increased sensitivity to bortezomib.
Inge Oudaert, Lauren van den Broecke, Osman Aksoy, Judith Lind, Sonia Vallet, Arne Van der Vreken, Gamze Ates, Ann Massie, Ken Maes, Kim De Veirman, Elke De Bruyne, Karin Vanderkerken, Klaus Podar, Eline Menu   +13 more
wiley   +1 more source

Tacrolimus may play a role in dermatitis and radiation-induced skin injury through cellular senescence

Radiation Medicine and Protection
Skin Exposure of skin to ionizing radiation can induce acute or chronic biological effects, resulting in radiation-induced skin injury (RSI). Premature cellular senescence, caused by oxidative stress and/or DNA damage from chemical or physical agents ...
Jie Chen, Ling Gao
doaj   +1 more source

Suppression of TCAB1 expression induced cellular senescence by lessening proteasomal degradation of p21 in cancer cells [PDF]

, 2021
Jing Niu, Ruiqi Gao, Mengtian Cui, Chenguang Zhang, Shentao Li, Shan Cheng, Wei Ding   +6 more
openalex   +1 more source

In vitro properties of patient serum predict clinical outcome after high dose rate brachytherapy of hepatocellular carcinoma

Molecular Oncology, EarlyView.
Following high dose rate brachytherapy (HDR‐BT) for hepatocellular carcinoma (HCC), patients were classified as responders and nonresponders. Post‐therapy serum induced increased BrdU incorporation and Cyclin E expression of Huh7 and HepG2 cells in nonresponders, but decreased levels in responders.
Lukas Salvermoser, Jan Niklas Schäfer, Shraga Nahum Goldberg, Philipp Maximilian Kazmierczak, Moritz Nikolaus Gröper, Philipp Franz Linden, Elif Öcal, Tanja Burkard, Stefanie Corradini, Najib Ben Khaled, Moritz Wildgruber, Max Seidensticker, Jens Ricke, Matthias Stechele, Marianna Alunni‐Fabbroni   +14 more
wiley   +1 more source

Autophagy: an adaptive physiological countermeasure to cellular senescence and ischaemia/reperfusion‐associated cardiac arrhythmias

, 2016
István Lekli, David Haines, György Balla, Árpád Tósaki   +3 more
openalex   +1 more source

A synthetic benzoxazine dimer derivative targets c‐Myc to inhibit colorectal cancer progression

Molecular Oncology, EarlyView.
Benzoxazine dimer derivatives bind to the bHLH‐LZ region of c‐Myc, disrupting c‐Myc/MAX complexes, which are evaluated from SAR analysis. This increases ubiquitination and reduces cellular c‐Myc. Impairing DNA repair mechanisms is shown through proteomic analysis.
Nicharat Sriratanasak, Bodee Nutho, Worawat Wattanathana, Narumon Phaonakrop, Bunnatut Panasawatwong, Katharina Erlenbach‐Wuensch, Sittiruk Roytrakul, Regine Schneider‐Stock, Pithi Chanvorachote   +8 more
wiley   +1 more source

The miR-30-5p/TIA-1 axis directs cellular senescence by regulating mitochondrial dynamics

Cell Death and Disease
Senescent cells exhibit a diverse spectrum of changes in their morphology, proliferative capacity, senescence-associated secretory phenotype (SASP) production, and mitochondrial homeostasis.
Hyosun Tak, Seongho Cha, Youlim Hong, Myeongwoo Jung, Seungyeon Ryu, Sukyoung Han, Seung Min Jeong, Wook Kim, Eun Kyung Lee   +8 more
doaj   +1 more source

Adaptaquin is selectively toxic to glioma stem cells through disruption of iron and cholesterol metabolism

Molecular Oncology, EarlyView.
Adaptaquin selectively kills glioma stem cells while sparing differentiated brain cells. Transcriptomic and proteomic analyses show Adaptaquin disrupts iron and cholesterol homeostasis, with iron chelation amplifying cytotoxicity via cholesterol depletion, mitochondrial dysfunction, and elevated reactive oxygen species.
Adrien M. Vaquié, Davod R. Shah, Eliane E. S. Brechbühl, Michael McNicholas, Zhaoyang Xu, John H. Stockley, Laura Morcom, Diana Gold Diaz, Gemma C. Girdler, Rachel V. Seear, Gabriel Balmus, Rajiv R. Ratan, Harry Bulstrode, James A. Nathan, Manav Pathania, Kevin M. Brindle, David H. Rowitch   +16 more
wiley   +1 more source