title: Targeting cancer stem-like cells in glioblastoma and colorectal cancer through metabolic pathways.
abstract: Cancer stem-like cells (CSCs) are thought to be the main cause of tumor occurrence, progression and therapeutic resistance. Strong research efforts in the last decade have led to the development of several tailored approaches to target CSCs with some very promising clinical trials underway; however, until now no anti-CSC therapy has been approved for clinical use. Given the recent improvement in our understanding of how onco-proteins can manipulate cellular metabolic networks to promote tumorigenesis, cancer metabolism research may well lead to innovative strategies to identify novel regulators and downstream mediators of CSC maintenance. Interfering with distinct stages of CSC-associated metabolics may elucidate novel, more efficient strategies to target this highly malignant cell population. Here recent discoveries regarding the metabolic properties attributed to CSCs in glioblastoma (GBM) and malignant colorectal cancer (CRC) were summarized. The association between stem cell markers, the response to hypoxia and other environmental stresses including therapeutic insults as well as developmentally conserved signaling pathways with alterations in cellular bioenergetic networks were also discussed. The recent developments in metabolic imaging to identify CSCs were also summarized. This summary should comprehensively update basic and clinical scientists on the metabolic traits of CSCs in GBM and malignant CRC.
authors.affiliation: Department of Neurosurgery, Heinrich-Heine University Medical Center, Düsseldorf, Germany.
authors.forename: U D
authors.initials: UD
authors.lastname: Kahlert
authors.affiliation: Department of Biology, University of Waterloo, Waterloo, ON, Canada.
authors.forename: S M
authors.initials: SM
authors.lastname: Mooney
authors.affiliation: Department of Neurosurgery, Brain Research Institute, Niigata University, Niigata, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Natsumeda
authors.affiliation: Department of Neurosurgery, Heinrich-Heine University Medical Center, Düsseldorf, Germany.
authors.forename: H-J
authors.initials: HJ
authors.lastname: Steiger
authors.affiliation: Department of Neurosurgery, Heinrich-Heine University Medical Center, Düsseldorf, Germany.
authors.forename: J
authors.initials: J
authors.lastname: Maciaczyk
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology / Q000627:therapeutic use; D014408:Biomarkers, Tumor / Q000378:metabolism; D001932:Brain Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D015687:Cell Hypoxia / Q000187:drug effects; D002986:Clinical Trials as Topic; D015179:Colorectal Neoplasms / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D005909:Glioblastoma / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D006801:Humans; D053858:Metabolic Networks and Pathways / Q000187:drug effects*; D058990:Molecular Targeted Therapy / Q000379:methods*; D014411:Neoplastic Stem Cells / Q000187:drug effects* / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D000970:Antineoplastic Agents; D014408:Biomarkers, Tumor
keywords: CD133; CD44; Notch; WNT; cancer stem cell; glutamate; glycine; hypoxia; metabolism; spectroscopy