Lipid Metabolism and Resistance to Anticancer Treatment DOI Creative Commons
Nicolas Germain,

Mélanie Dhayer,

M. Boileau

et al.

Biology, Journal Year: 2020, Volume and Issue: 9(12), P. 474 - 474

Published: Dec. 16, 2020

Metabolic reprogramming is crucial to respond cancer cell requirements during tumor development. In the last decade, metabolic alterations have been shown modulate cells’ sensitivity chemotherapeutic agents including conventional and targeted therapies. Recently, it became apparent that changes in lipid metabolism represent important mediators of resistance anticancer agents. this review, we highlight associated with therapy resistance, their significance how dysregulated could be exploited overcome drug resistance.

Language: Английский

The role of ROS in tumour development and progression DOI
Eric C. Cheung, Karen H. Vousden

Nature reviews. Cancer, Journal Year: 2022, Volume and Issue: 22(5), P. 280 - 297

Published: Jan. 31, 2022

Language: Английский

Citations

987

The double-edged roles of ROS in cancer prevention and therapy DOI Creative Commons

Yawei Wang,

Huan Qi, Yu Liu

et al.

Theranostics, Journal Year: 2021, Volume and Issue: 11(10), P. 4839 - 4857

Published: Jan. 1, 2021

Reactive oxygen species (ROS) serve as cell signaling molecules generated in oxidative metabolism and are associated with a number of human diseases. The reprogramming redox induces abnormal accumulation ROS cancer cells. It has been widely accepted that play opposite roles tumor growth, metastasis apoptosis according to their different distributions, concentrations durations specific subcellular structures. These double-edged progression include the ROS-dependent malignant transformation stress-induced death. In this review, we summarize notable literatures on generation scavenging, discuss related signal transduction networks corresponding anticancer therapies. There is no doubt an improved understanding sophisticated mechanism biology imperative conquer cancer.

Language: Английский

Citations

430

Mechanisms of Metabolic Reprogramming in Cancer Cells Supporting Enhanced Growth and Proliferation DOI Creative Commons
Chelsea Schiliro, Bonnie L. Firestein

Cells, Journal Year: 2021, Volume and Issue: 10(5), P. 1056 - 1056

Published: April 29, 2021

Cancer cells alter metabolic processes to sustain their characteristic uncontrolled growth and proliferation. These alterations include (1) a shift from oxidative phosphorylation aerobic glycolysis support the increased need for ATP, (2) glutaminolysis NADPH regeneration, (3) altered flux through pentose phosphate pathway tricarboxylic acid cycle macromolecule generation, (4) lipid uptake, lipogenesis, cholesterol synthesis, (5) upregulation of one-carbon metabolism production NADH/NADPH, nucleotides, glutathione, (6) amino metabolism, (7) metabolism-based regulation apoptosis, (8) utilization alternative substrates, such as lactate acetate. Altered in cancer is controlled by tumor-host cell interactions, key oncogenes, tumor suppressors, other regulatory molecules, including non-coding RNAs. Changes pathways are dynamic, exhibit plasticity, often dependent on type microenvironment, leading thought Warburg Effect "reverse Effect" plasticity. Understanding complex nature these multiple can development new therapies.

Language: Английский

Citations

374

Phosphorylated NFS1 weakens oxaliplatin-based chemosensitivity of colorectal cancer by preventing PANoptosis DOI Creative Commons

Jin‐Fei Lin,

Peishan Hu,

Yiyu Wang

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2022, Volume and Issue: 7(1)

Published: Feb. 28, 2022

Metabolic enzymes have an indispensable role in metabolic reprogramming, and their aberrant expression or activity has been associated with chemosensitivity. Hence, targeting remains attractive approach for treating tumors. However, the influence regulation of cysteine desulfurase (NFS1), a rate-limiting enzyme iron-sulfur (Fe-S) cluster biogenesis, colorectal cancer (CRC) remain elusive. Here, using vivo gene-based clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 library screen, we revealed that loss NFS1 significantly enhanced sensitivity CRC cells to oxaliplatin. In vitro results showed deficiency synergizing oxaliplatin triggered PANoptosis (apoptosis, necroptosis, pyroptosis, ferroptosis) by increasing intracellular levels reactive oxygen species (ROS). Furthermore, oxaliplatin-based oxidative stress phosphorylation level serine residues NFS1, which prevented S293 phosphorylation-dependent manner during treatment. addition, high transcriptionally regulated MYC, was found tumor tissues poor survival hyposensitivity chemotherapy patients CRC. Overall, findings this study provided insights into underlying mechanisms identified inhibition as promising strategy improving outcome platinum-based treatment

Language: Английский

Citations

189

Lactate and glutamine support NADPH generation in cancer cells under glucose deprived conditions DOI Creative Commons
Minfeng Ying,

Duo You,

Xiaobing Zhu

et al.

Redox Biology, Journal Year: 2021, Volume and Issue: 46, P. 102065 - 102065

Published: July 11, 2021

Although glucose, through pentose phosphate pathway (PPP), is the main source to generate NADPH, solid tumors are often deprived of hence alternative metabolic pathways maintain NADPH homeostasis in cancer cells required. Here, we report that lactate and glutamine support production via isocitrate dehydrogenase 1 (IDH1) malic enzyme (ME1), respectively, under glucose-deprived conditions. Isotopic tracing demonstrates participates formation isocitrate. Malate derived from mitochondria shuttles cytosol produce NADPH. In cultured absence knockout IDH1 ME1 decreases NADPH/NADP+ GSH/GSSG, increases ROS level facilitates cell necrosis. 4T1 murine breast tumors, retards tumor growth vivo, with combined ME1/IDH1 more strongly suppressing growth. Our findings reveal two NADPH-producing use resist glucose starvation, reflecting plasticity flexibility adapting nutrition stress.

Language: Английский

Citations

118

Stimuli-Responsive Polymer-Based Nanosystems for Cancer Theranostics DOI
Dengshuai Wei, Yong Sun,

Hu Zhu

et al.

ACS Nano, Journal Year: 2023, Volume and Issue: 17(23), P. 23223 - 23261

Published: Dec. 2, 2023

Stimuli-responsive polymers can respond to internal stimuli, such as reactive oxygen species (ROS), glutathione (GSH), and pH, biological enzymes, external lasers ultrasound, etc., by changing their hydrophobicity/hydrophilicity, degradability, ionizability, thus have been widely used in biomedical applications. Due the characteristics of tumor microenvironment (TME), stimuli-responsive that cater specifically TME extensively prepare smart nanovehicles for targeted delivery therapeutic diagnostic agents tissues. Compared conventional drug nanosystems, TME-responsive nanosystems many advantages, high sensitivity, broad applicability among different tumors, functional versatility, improved biosafety. In recent years, a great deal research has devoted engineering efficient polymeric significant improvement made both cancer diagnosis therapy. this review, we summarize some advances involving use polymer nanocarriers delivery, imaging, therapy, theranostics. Various chemical stimuli will be described context nanosystems. Accordingly, groups responsible responsiveness strategies incorporate these into discussed detail. With on topic expending at fast pace, innovative concepts, sequential cascade release, NIR-II multifunctional formulations, emerged popular enhanced performance, which also included here with up-to-date illustrations. We hope review offer valuable insights selection optimization help accelerate future applications treatment.

Language: Английский

Citations

117

Emerging therapies in cancer metabolism DOI Creative Commons
Yi Xiao, Tian‐Jian Yu, Ying Xu

et al.

Cell Metabolism, Journal Year: 2023, Volume and Issue: 35(8), P. 1283 - 1303

Published: Aug. 1, 2023

Language: Английский

Citations

96

Blocking glutathione regeneration: Inorganic NADPH oxidase nanozyme catalyst potentiates tumoral ferroptosis DOI
Chenyao Wu,

Deliang Xu,

Min Ge

et al.

Nano Today, Journal Year: 2022, Volume and Issue: 46, P. 101574 - 101574

Published: Aug. 5, 2022

Language: Английский

Citations

83

PANoptosis: Mechanisms, biology, and role in disease DOI Open Access

Xu Sun,

Yanpeng Yang,

Xiaona Meng

et al.

Immunological Reviews, Journal Year: 2023, Volume and Issue: 321(1), P. 246 - 262

Published: Oct. 12, 2023

Summary Cell death can be executed through distinct subroutines. PANoptosis is a unique inflammatory cell modality involving the interactions between pyroptosis, apoptosis, and necroptosis, which mediated by multifaceted PANoptosome complexes assembled via integrating components from other modalities. There growing interest in process function of PANoptosis. Accumulating evidence suggests that occurs under diverse stimuli, for example, viral or bacterial infection, cytokine storm, cancer. Given impact across disease spectrum, this review briefly describes relationships highlights key molecules formation activation, outlines roles diseases together with potential therapeutic targeting. We also discuss important concepts pressing issues future research. Improved understanding its mechanisms crucial identifying novel targets strategies.

Language: Английский

Citations

71

Targeting oxidative stress as a preventive and therapeutic approach for cardiovascular disease DOI Creative Commons
Yan Qian, Shasha Liu, Yang Sun

et al.

Journal of Translational Medicine, Journal Year: 2023, Volume and Issue: 21(1)

Published: Aug. 2, 2023

Abstract Cardiovascular diseases (CVDs) continue to exert a significant impact on global mortality rates, encompassing conditions like pulmonary arterial hypertension (PAH), atherosclerosis (AS), and myocardial infarction (MI). Oxidative stress (OS) plays crucial role in the pathogenesis advancement of CVDs, highlighting its significance as contributing factor. Maintaining an equilibrium between reactive oxygen species (ROS) antioxidant systems not only aids mitigating oxidative but also confers protective benefits cardiac health. Herbal monomers can inhibit OS CVDs by activating multiple signaling pathways, such increasing activity endogenous decreasing level ROS expression. Given actions herbal significantly protect normal function heart reduce damage caused organism. Hence, it is imperative recognize prospective therapeutic interventions for CVDs. This paper aims comprehensively review origins mechanisms underlying OS, elucidate intricate association explore potential treatment utilizing monomers. Furthermore, particular emphasis will be placed examining cardioprotective effects evaluating their pathways subsequent treatment. Graphical

Language: Английский

Citations

69