title: Human cancer: is it linked to dysfunctional lipid metabolism?
abstract: BACKGROUND
  Lipid metabolism dysfunction leading to excess fat deposits (obesity) may cause tumor (cancer) development. Both obesity and cancer are the epicenter of important medical issues. Lipid metabolism and cell death/proliferation are controlled by biochemical and molecular pathways involving many proteins, and organelles; alteration in these pathways leads to fat accumulation or tumor growth. Mammalian Krüppel-like factors, KLFs play key roles in both lipid metabolism and tumor development.
  
  
  METHODS
  Substantial epidemiological and clinical studies have established strong association of obesity with a number of human cancers. However, we need more experimental verification to determine the exact role of this metabolic alteration in the context of tumor development. A clear understanding of molecules, pathways and the mechanisms involved in lipid metabolism and cell death/proliferation will have important implications in pathogenesis, and prevention of these diseases.
  
  
  CONCLUSIONS
  The regulatory role of KLFs, in both cell death/proliferation and lipid metabolism suggests a common regulation of both processes. This provides an excellent model for delivering a precise understanding of the mechanisms linking altered expression of KLFs to obesity and tumor development.
  
  
  CONCLUSIONS
  Currently, mouse and rats are the models of choice for investigating disease mechanisms and pharmacological therapies but a genetic model is needed for a thorough examination of KLF function in vivo during the development of an organism. The worm Caenorhabditis elegans is an ideal model to study the connectivity between lipid metabolism and cell death/proliferation.
authors.affiliation: Developmental Biology, Center for Vector Biology, Rutgers University, New Brunswick, NJ 08901, United States. Electronic address: sarwar.hashmi@rutgers.edu.
authors.forename: Sarwar
authors.initials: S
authors.lastname: Hashmi
authors.affiliation: Developmental Biology, Center for Vector Biology, Rutgers University, New Brunswick, NJ 08901, United States.
authors.forename: Yi
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Developmental Biology, Center for Vector Biology, Rutgers University, New Brunswick, NJ 08901, United States.
authors.forename: Devi S
authors.initials: DS
authors.lastname: Suman
authors.affiliation: Department of Cell Biology, KFSH&RC, Riyadh 11211, Saudi Arabia.
authors.forename: Ranjit S
authors.initials: RS
authors.lastname: Parhar
authors.affiliation: Department of Cell Biology, KFSH&RC, Riyadh 11211, Saudi Arabia.
authors.forename: Kate
authors.initials: K
authors.lastname: Collison
authors.affiliation: Department of Cell Biology, KFSH&RC, Riyadh 11211, Saudi Arabia.
authors.forename: Walter
authors.initials: W
authors.lastname: Conca
authors.affiliation: Department of Cell Biology, KFSH&RC, Riyadh 11211, Saudi Arabia.
authors.forename: Futwan
authors.initials: F
authors.lastname: Al-Mohanna
authors.affiliation: Developmental Biology, Center for Vector Biology, Rutgers University, New Brunswick, NJ 08901, United States.
authors.forename: Randy
authors.initials: R
authors.lastname: Gaugler
mesh_terms: D000818:Animals; D017173:Caenorhabditis elegans; D016923:Cell Death; D049109:Cell Proliferation; D006801:Humans; D050356:Lipid Metabolism; D051379:Mice; D009369:Neoplasms / Q000453:epidemiology / Q000378:metabolism / Q000473:pathology / Q000628:therapy; D009765:Obesity / Q000453:epidemiology / Q000378:metabolism / Q000473:pathology / Q000628:therapy; D051381:Rats
keywords: Apoptosis; Cancer; Krüppel-like factor; Lipid metabolism; Obesity; Tumor development