Nature Cancer, Journal Year: 2023, Volume and Issue: 4(6), P. 829 - 843
Published: June 5, 2023
Language: Английский
Nature Reviews Drug Discovery, Journal Year: 2020, Volume and Issue: 19(7), P. 480 - 494
Published: June 17, 2020
Language: Английский
Citations
615
Signal Transduction and Targeted Therapy, Journal Year: 2022, Volume and Issue: 7(1)
Published: Aug. 13, 2022
Regulated cell death (RCD), also well-known as programmed (PCD), refers to the form of that can be regulated by a variety biomacromolecules, which is distinctive from accidental (ACD). Accumulating evidence has revealed RCD subroutines are key features tumorigenesis, may ultimately lead establishment different potential therapeutic strategies. Hitherto, targeting with pharmacological small-molecule compounds been emerging promising avenue, rapidly progressed in many types human cancers. Thus, this review, we focus on summarizing not only apoptotic and autophagy-dependent signaling pathways, but crucial pathways other subroutines, including necroptosis, pyroptosis, ferroptosis, parthanatos, entosis, NETosis lysosome-dependent (LCD) cancer. Moreover, further discuss current situation several improve cancer treatment, such single-target, dual or multiple-target compounds, drug combinations, some new strategies would together shed light future directions attack vulnerabilities drugs for purposes.
Language: Английский
Citations
502
Nature Reviews Drug Discovery, Journal Year: 2022, Volume and Issue: 22(3), P. 213 - 234
Published: Dec. 12, 2022
Language: Английский
Citations
253
Cell, Journal Year: 2020, Volume and Issue: 183(4), P. 860 - 874
Published: Nov. 1, 2020
Language: Английский
Citations
223
Signal Transduction and Targeted Therapy, Journal Year: 2020, Volume and Issue: 5(1)
Published: Oct. 7, 2020
Abstract Resistance to cancer therapy is a major barrier management. Conventional views have proposed that acquisition of resistance may result from genetic mutations. However, accumulating evidence implicates key role non-mutational mechanisms underlying drug tolerance, the latter which focus will be discussed here. Such processes are largely driven by tumor cell plasticity, renders cells insusceptible drug-targeted pathway, thereby facilitating survival and growth. The concept plasticity highlights significance re-activation developmental programs closely correlated with epithelial–mesenchymal transition, properties stem cells, trans-differentiation potential during exposure. From observations in various cancers, this provides an opportunity for investigating nature anticancer resistance. Over years, our understanding emerging phenotype switching modifying therapeutic response has considerably increased. This expanded knowledge contributes developing novel strategies or combination regimens using available drugs, likely improve patient outcomes clinical practice.
Language: Английский
Citations
198
Molecular Cell, Journal Year: 2020, Volume and Issue: 78(6), P. 1002 - 1018
Published: June 1, 2020
Language: Английский
Citations
155
Nature Cancer, Journal Year: 2022, Volume and Issue: unknown
Published: Dec. 23, 2022
Language: Английский
Citations
148
Annual Review of Pathology Mechanisms of Disease, Journal Year: 2020, Volume and Issue: 16(1), P. 299 - 322
Published: Nov. 25, 2020
Studies of the regenerative capacity liver have converged on Hippo pathway, a serine/threonine kinase cascade discovered in Drosophila and conserved from unicellular organisms to mammals. Genetic studies mouse rat livers revealed that pathway is key regulator size, regeneration, development, metabolism, homeostasis perturbations can lead development common diseases, such as fatty disease cancer. In turn, pharmacological targeting may be utilized boost regeneration prevent progression diseases. We review current insights provided by into pathophysiology. Furthermore, we present path forward for future understand how newly identified components control physiology regulated liver.
Language: Английский
Citations
147
Science Translational Medicine, Journal Year: 2020, Volume and Issue: 12(559)
Published: Sept. 2, 2020
Acquired resistance to tyrosine kinase inhibitors (TKIs) of epidermal growth factor receptor (EGFR) remains a clinical challenge. Especially challenging are cases in which emerges through EGFR-independent mechanisms, such as pathways that promote epithelial-to-mesenchymal transition (EMT). Through an integrated transcriptomic, proteomic, and drug screening approach, we identified activation the yes-associated protein (YAP) forkhead box M1 (FOXM1) axis driver EMT-associated EGFR TKI resistance. inhibitor was associated with broad multidrug extended across multiple chemotherapeutic targeted agents, consistent difficulty effectively treating resistant disease. TKI-resistant cells displayed increased abundance spindle assembly checkpoint (SAC) proteins, including polo-like 1 (PLK1), Aurora kinases, survivin, kinesin (KSP). Moreover, exhibited vulnerability SAC inhibitors. Increased YAP/FOXM1 mediated increase components cells. The relevance these finding indicated by evaluation specimens from patients mutant lung cancer, showed high FOXM1 expression correlated genes encoding proteins worse outcome. These data revealed central regulator this pathway, along components, therapeutic vulnerabilities for targeting multidrug-resistant phenotype.
Language: Английский
Citations
145
Nature, Journal Year: 2022, Volume and Issue: 608(7924), P. 784 - 794
Published: July 7, 2022
Language: Английский
Citations
133