c-Myc and Cancer Metabolism DOI Open Access
Donald M. Miller, Shelia D. Thomas,

Ashraful Islam

et al.

Clinical Cancer Research, Journal Year: 2012, Volume and Issue: 18(20), P. 5546 - 5553

Published: Oct. 14, 2012

The processes of cellular growth regulation and metabolism are closely interrelated. c-Myc oncogene is a "master regulator" which controls many aspects both these processes. metabolic changes occur in transformed cells, driven by overexpression, necessary to support the increased need for nucleic acids, proteins, lipids rapid proliferation. At same time, overexpression results coordinated level expression gene families result This interesting duality effects places it mainstream transformational gives very important role regulating "transformed phenotype." induced can either as "primary oncogene" activated amplification or translocation downstream effect other oncogenes. In case, appears that plays central sustaining with transformation. Although efforts use therapeutic target have been quite frustrating, this may change next few years.

Language: Английский

Energy metabolism of cancer: Glycolysis versus oxidative phosphorylation (Review) DOI Open Access
Jie Zheng

Oncology Letters, Journal Year: 2012, Volume and Issue: 4(6), P. 1151 - 1157

Published: Jan. 1, 2012

Metabolic activities in normal cells rely primarily on mitochondrial oxidative phosphorylation (OXPHOS) to generate ATP for energy. Unlike cells, glycolysis is enhanced and OXPHOS capacity reduced various cancer cells. It has long been believed that the glycolytic phenotype due a permanent impairment of OXPHOS, as proposed by Otto Warburg. This view challenged recent investigations which find function most cancers intact. Aerobic many combined result factors such oncogenes, tumor suppressors, hypoxic microenvironment, mtDNA mutations, genetic background others. Understanding features complexity energy metabolism will help develop new approaches early diagnosis effectively target therapy cancer.

Language: Английский

Citations

830

The Role of Snail in EMT and Tumorigenesis DOI
Yifan Wang, Jian Shi,

Kequn Chai

et al.

Current Cancer Drug Targets, Journal Year: 2013, Volume and Issue: 13(9), P. 963 - 972

Published: Dec. 31, 2013

Epithelial-mesenchymal transition (EMT) is a highly conserved process in which polarized, immobile epithelial cells lose tight junctions, associated adherence, and become migratory mesenchymal cells. Several transcription factors, including the Snail/Slug family, Twist, δEF1/ZEB1, SIP1/ZEB2 E12/E47 respond to microenvironmental stimuli function as molecular switches for EMT program. Snail zinc-finger transcriptional repressor controlling during embryogenesis tumor progression. Through its N-terminal SNAG domain, interacts with several corepressors epigenetic remodeling complexes repress specific target genes, such E-cadherin gene (CDH1). An integrated complex signaling network, RTKs, TGF-β, Notch, Wnt, TNF-α, BMPs pathways, activates Snail, thereby inducing EMT. expression correlates grade, nodal metastasis of many types predicts poor outcome patients metastatic cancer. Emerging evidences indicate that causes metabolic reprogramming, bestows cancer stem cell-like traits, additionally, promotes drug resistance, recurrence metastasis. Despite new exciting developments, challenges remain be addressed order understand more thoroughly role Additional investigations are required disclose contribution factors on This information will lead comprehensive understanding provide us novel approaches preventing treating cancers. Keywords: Breast cancer, EMT, metastasis, pathway, snail.

Language: Английский

Citations

810

ERK1/2-dependent phosphorylation and nuclear translocation of PKM2 promotes the Warburg effect DOI
Weiwei Yang, Yanhua Zheng, Yan Xia

et al.

Nature Cell Biology, Journal Year: 2012, Volume and Issue: 14(12), P. 1295 - 1304

Published: Nov. 25, 2012

Language: Английский

Citations

795

Cellular Metabolism and Disease: What Do Metabolic Outliers Teach Us? DOI Creative Commons
Ralph J. DeBerardinis, Craig B. Thompson

Cell, Journal Year: 2012, Volume and Issue: 148(6), P. 1132 - 1144

Published: March 1, 2012

Language: Английский

Citations

790

c-Myc and Cancer Metabolism DOI Open Access
Donald M. Miller, Shelia D. Thomas,

Ashraful Islam

et al.

Clinical Cancer Research, Journal Year: 2012, Volume and Issue: 18(20), P. 5546 - 5553

Published: Oct. 14, 2012

The processes of cellular growth regulation and metabolism are closely interrelated. c-Myc oncogene is a "master regulator" which controls many aspects both these processes. metabolic changes occur in transformed cells, driven by overexpression, necessary to support the increased need for nucleic acids, proteins, lipids rapid proliferation. At same time, overexpression results coordinated level expression gene families result This interesting duality effects places it mainstream transformational gives very important role regulating "transformed phenotype." induced can either as "primary oncogene" activated amplification or translocation downstream effect other oncogenes. In case, appears that plays central sustaining with transformation. Although efforts use therapeutic target have been quite frustrating, this may change next few years.

Language: Английский

Citations

773