Nature, Journal Year: 2019, Volume and Issue: 566(7744), P. 403 - 406
Published: Feb. 6, 2019
Language: Английский
Nature, Journal Year: 2019, Volume and Issue: 566(7744), P. 403 - 406
Published: Feb. 6, 2019
Language: Английский
Cell, Journal Year: 2016, Volume and Issue: 166(3), P. 555 - 566
Published: July 1, 2016
Language: Английский
Citations
1426Nature Cell Biology, Journal Year: 2018, Volume and Issue: 20(7), P. 745 - 754
Published: June 22, 2018
Language: Английский
Citations
1374Nature reviews. Cancer, Journal Year: 2016, Volume and Issue: 16(11), P. 732 - 749
Published: Sept. 23, 2016
Language: Английский
Citations
1294Nature Cell Biology, Journal Year: 2015, Volume and Issue: 17(4), P. 351 - 359
Published: March 16, 2015
Language: Английский
Citations
1292British Journal of Cancer, Journal Year: 2019, Volume and Issue: 122(1), P. 4 - 22
Published: Dec. 10, 2019
Abstract A common feature of cancer cells is their ability to rewire metabolism sustain the production ATP and macromolecules needed for cell growth, division survival. In particular, importance altered fatty acid in has received renewed interest as, aside principal role as structural components membrane matrix, they are important secondary messengers, can also serve fuel sources energy production. this review, we will examine mechanisms through which with a focus on four main areas research. (1) The de novo synthesis exogenous uptake cellular pool acids. (2) molecular heterogeneity oncogenic signal transduction pathways, such PI3K–AKT–mTOR signalling, regulate metabolism. (3) acids essential mediators progression metastasis, remodelling tumour microenvironment. (4) Therapeutic strategies considerations successfully targeting cancer. Further research focusing complex interplay between signalling dysregulated holds great promise uncover novel metabolic vulnerabilities improve efficacy targeted therapies.
Language: Английский
Citations
1183Cell Death and Disease, Journal Year: 2016, Volume and Issue: 7(6), P. e2253 - e2253
Published: June 9, 2016
Abstract Tumor cells harbor genetic alterations that promote a continuous and elevated production of reactive oxygen species. Whereas such oxidative stress conditions would be harmful to normal cells, they facilitate tumor growth in multiple ways by causing DNA damage genomic instability, ultimately, reprogramming cancer cell metabolism. This review outlines the metabolic-dependent mechanisms tumors engage when faced with are critical for progression producing redox cofactors. In particular, we describe how mitochondria has key role regulating interplay between homeostasis metabolism within cells. Last, will discuss potential therapeutic use agents directly or indirectly block
Language: Английский
Citations
995Nature Reviews Molecular Cell Biology, Journal Year: 2015, Volume and Issue: 16(7), P. 393 - 405
Published: June 23, 2015
Language: Английский
Citations
993Nature Neuroscience, Journal Year: 2020, Volume and Issue: 23(2), P. 194 - 208
Published: Jan. 20, 2020
Language: Английский
Citations
894Developmental Cell, Journal Year: 2015, Volume and Issue: 32(6), P. 678 - 692
Published: March 1, 2015
Language: Английский
Citations
853Annual Review of Physiology, Journal Year: 2019, Volume and Issue: 82(1), P. 103 - 126
Published: Nov. 15, 2019
Acidic metabolic waste products accumulate in the tumor microenvironment because of high activity and insufficient perfusion. In tumors, acidity interstitial space relatively well-maintained intracellular pH influence cancer stromal cell function, their mutual interplay, interactions with extracellular matrix. Tumor is spatially temporally heterogeneous, fitness advantage cells adapted to likely particularly evident when they encounter less acidic regions, for instance, during invasion. Through complex effects on genetic stability, epigenetics, cellular metabolism, proliferation, survival, compartmentalized favors development. Cellular selection exacerbates malignant phenotype, which further enhanced by acid-induced motility, matrix degradation, attenuated immune responses, modified intercellular signaling. this review, we discuss how influences each stage development, from dysplasia full-blown metastatic disease.
Language: Английский
Citations
847