Article
Biochemistry & Molecular Biology
Xin-fang Jie, Yun-peng Li, Shuai Liu, Yue Fu, Yuan-yuan Xiong
Summary: This study investigated the effect of miR-491-5p on ferroptosis in glioblastoma (GBM). The results showed that miR-491-5p interfered with TP53 through the p53/p21 pathway and reduced the sensitivity of GBM to ferroptosis.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2023)
Article
Biology
Amy Tarangelo, Jason Rodencal, Joon Tae Kim, Leslie Magtanong, Jonathan Z. Long, Scott J. Dixon
Summary: Nucleotide synthesis is essential for DNA replication and other cellular processes. Inhibiting nucleotide metabolism can suppress non-apoptotic cell death, such as ferroptosis. The study reveals that inhibition of nucleotide metabolism through the p53 pathway can prevent ferroptosis by stabilizing wild-type p53 and inducing the p53 target gene CDKN1A (p21) to decrease the expression of ribonucleotide reductase subunits RRM1 and RRM2.
LIFE SCIENCE ALLIANCE
(2022)
Article
Multidisciplinary Sciences
Delin Chen, Bo Chu, Xin Yang, Zhaoqi Liu, Ying Jin, Ning Kon, Raul Rabadan, Xuejun Jiang, Brent R. Stockwell, Wei Gu
Summary: The study identifies iPLA2 beta as a critical regulator for p53-driven ferroptosis independent of GPX4. Loss of iPLA2 beta does not have obvious effect on normal cells, but it plays an essential role in regulating ferroptosis upon ROS-induced stress. iPLA2 beta is a promising therapeutic target for activating ferroptosis-mediated tumor suppression without serious toxicity concerns.
NATURE COMMUNICATIONS
(2021)
Article
Multidisciplinary Sciences
Erdem M. Terzi, Vladislav O. Sviderskiy, Samantha W. Alvarez, Gabrielle C. Whiten, Richard Possemato
Summary: Intracellular iron levels are strictly regulated to avoid iron-mediated ROS production. Loss of ISC synthesis can activate IRP2 independently of IRP1 and FBXL5, promoting ferroptosis sensitivity. Deletion of both IRP1 and IRP2 abolishes the iron-starvation response, preventing its activation by ISC synthesis inhibition.
Article
Cell Biology
Akira Koyanagi, Hitoshi Kotani, Yuichi Iida, Ryosuke Tanino, Irna D. Kartika, Koji Kishimoto, Mamoru Harada
Summary: Cytoplasmic p21 protein in therapy-induced lung cancer cells plays a protective role in cell death, mainly by inhibiting cellular senescence and promoting ferroptosis. Loss of p21 protein increases the sensitivity of lung cancer cells to therapy.
CELL PROLIFERATION
(2022)
Article
Biochemistry & Molecular Biology
Guang Lei, Yilei Zhang, Ting Hong, Xudong Zhang, Xiaoguang Liu, Chao Mao, Yuelong Yan, Pranavi Koppula, Weijie Cheng, Anil K. Sood, Jinsong Liu, Boyi Gan
Summary: The study reveals the critical role of ferroptosis in p53-mediated tumor radiosensitivity, promoting lipid peroxidation and cell death by inhibiting SLC7A11. P53 deficiency leads to radioresistance in cancer cells or tumors, while ferroptosis inducers that inhibit SLC7A11 significantly enhance tumor sensitivity to radiotherapy.
Review
Medicine, Research & Experimental
Ling Xu, Yu 'e Liu, Xi Chen, Hua Zhong, Yi Wang
Summary: Ferroptosis is a novel type of programmed cell death characterized by dysregulated iron metabolism and accumulation of lipid peroxides. It plays a critical role in cancers and other diseases, inhibiting the proliferation of malignant cells and offering potential as a new method of cancer treatment. Inhibitors targeting key factors of ferroptosis have been developed and the application of ferroptosis is focused on avoiding it in healthy cells and selectively inducing it in cancers.
BIOMEDICINE & PHARMACOTHERAPY
(2023)
Article
Cell Biology
Jia You, Siyu Ouyang, Zhongcheng Xie, Chenxi Zhi, Jiang Yu, Xiaoqian Tan, Pin Li, Xiaoyan Lin, Wentao Ma, Zhiyang Liu, Qin Hou, Nan Xie, Tianhong Peng, Xi Chen, Liang Li, Wei Xie
Summary: This study aimed to determine the effects of ferroptosis on atherosclerosis induced by lipid overload and its impact on vascular smooth muscle cells (VSMCs). It was found that the ferroptosis inhibitor Fer-1 could improve high plasma levels of triglycerides, total cholesterol, low-density lipoprotein, and glucose, and reduce atherosclerotic lesions in ApoE(-/-) mice. In addition, Fer-1 reduced iron accumulation in atherosclerotic lesions by affecting the expression of TFR1, FTH, and FTL in VSMCs.
JOURNAL OF CELLULAR PHYSIOLOGY
(2023)
Article
Obstetrics & Gynecology
Ting Zhao, Xiao Xiao, Lingchuan Li, Xiaomei Wu, Tao Yuan
Summary: The study investigated the effect of benzothiazole derivatives (Rosline) on ovarian cancer and its potential mechanism. The results showed that Rosline inhibited the proliferation of ovarian cancer cells and blocked the cell cycle progression. It promoted the expression of p21 through a p53-independent pathway, thereby inhibiting cell proliferation and blocking the cell cycle.
JOURNAL OF OBSTETRICS AND GYNAECOLOGY RESEARCH
(2023)
Review
Pharmacology & Pharmacy
Haixia Ji, Wenzhe Wang, Xia Li, Xiaoying Han, Xinyu Zhang, Juan Wang, Changxiao Liu, Luqi Huang, Wenyuan Gao
Summary: This review discusses the role of the p53 gene in regulating ferroptosis, primarily through influencing metabolic networks and signaling pathways that affect tumor cell sensitivity to ferroptosis. This has important implications for further understanding the role of p53 in tumor ferroptosis and developing new strategies for cancer treatment.
PHARMACOLOGICAL RESEARCH
(2022)
Article
Biochemistry & Molecular Biology
Fanen Yuan, Qian Sun, Si Zhang, Liguo Ye, Yang Xu, Gang Deng, Zhou Xu, Shenqi Zhang, Baohui Liu, Qianxue Chen
Summary: This study reveals a dual role of p62 in regulating ferroptosis in glioblastoma (GBM) depending on the status of p53. P62 overexpression promotes ferroptosis and inhibits SLC7A11 expression in p53 mutant GBM, while attenuates ferroptosis and promotes SLC7A11 expression in p53 wild-type GBM. The mutation status of p53 is a crucial factor in determining the therapeutic response to p62-mediated ferroptosis-targeted therapies in GBM.
CELL AND BIOSCIENCE
(2022)
Article
Biochemistry & Molecular Biology
Ukjin Kim, Kwang Seok Kim, Jong-Kuk Park, Hong -Duck Um
Summary: Based on previous findings, the interaction between p53 and p21 is essential for the tumor-suppressing functions of p53, and the acetylation of the C-terminal domain of p53 can affect this interaction. In this study, it was found that inhibiting the deacetylase SIRT1 or increasing the acetylation levels of lysine residues in the C-terminal domain reduced the interaction between p53 and p21. Additionally, substituting acetylation mimetics for the lysine residues in the C-terminal domain weakened the interaction. The degree of acetylation correlated with the extent of the inhibitory effect. Overall, these results suggest that cellular components involved in the acetylation or deacetylation of the C-terminal domain of p53 play a critical role in regulating the formation of the p53/p21 complex.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2022)
Review
Cell Biology
Fangze Huang, Ronghua Yang, Zezhou Xiao, Yu Xie, Xuefeng Lin, Peng Zhu, Pengyu Zhou, Jun Lu, Shaoyi Zheng
Summary: Ferroptosis, a novel form of non-apoptotic regulated cell death driven by iron and lethal lipid hydroperoxides, plays a critical role in the development of cardiovascular diseases. Recent studies have shown that ferroptosis inhibitors and other substances can alleviate myocardial injury by targeting the ferroptosis pathway.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Engineering, Mechanical
Jude Shalitha Perera, Nelson Lam
Summary: In hilly urban areas, reinforced concrete barriers with a layer of gabions are commonly used for hillslope protection. The gabions provide additional protection by avoiding localized failure caused by direct contact with fallen boulders, while also acting as a cushion to reduce momentum transfer and bending of the barrier wall. This study presents a new design procedure that considers the cushioning mechanism of gabions in multiple strike scenarios.
INTERNATIONAL JOURNAL OF IMPACT ENGINEERING
(2023)
Article
Cell Biology
Feng Gao, Bin Zhang, Zhanfa Sun, Yuan Gao, Chunyi Liu, Xueyong Dou, Haokun Tong, Rui Wang
Summary: This study found that Sestrins 1 (SESN1) plays an inhibitory role in vascular endothelial ferroptosis through the activation of P21 in atherosclerosis (AS). Experimental results from AS mouse models and cell models showed that overexpression of SESN1 can inhibit inflammatory response, oxidative stress response, and endothelial ferroptosis.