AustralieFrV1, PubMed, Checkpoint, bibRecord, 001E70

Expression of Cell-Surface Marker ABCB5 Causes Characteristic Modifications of Glucose, Amino Acid and Phospholipid Metabolism in the G3361 Melanoma-Initiating Cell Line.

Identifieur interne : 001E70 ( PubMed/Checkpoint ); précédent : 001E69; suivant : 001E71

Expression of Cell-Surface Marker ABCB5 Causes Characteristic Modifications of Glucose, Amino Acid and Phospholipid Metabolism in the G3361 Melanoma-Initiating Cell Line.

Auteurs : Norbert W. Lutz [France] ; Pallavi Banerjee [États-Unis] ; Brian J. Wilson [États-Unis] ; Jie Ma [États-Unis] ; Patrick J. Cozzone [France] ; Markus H. Frank [États-Unis]

Source :

PloS one [ 1932-6203 ] ; 2016.

RBID : pubmed:27560924

Descripteurs français

English descriptors

KwdEn :
- Alanine (metabolism), Amino Acids (metabolism), Biomarkers, Tumor (genetics), Biomarkers, Tumor (metabolism), Cell Line, Tumor, Cell Membrane (metabolism), Gene Expression Regulation, Neoplastic, Glucose (metabolism), Glycerylphosphorylcholine (metabolism), Humans, Lactates (metabolism), Magnetic Resonance Spectroscopy, Melanoma (genetics), Melanoma (metabolism), Melanoma (pathology), Metabolomics (methods), Neoplastic Stem Cells (metabolism), P-Glycoprotein (genetics), P-Glycoprotein (metabolism), Phosphatidylethanolamines (metabolism), Phospholipids (metabolism), Pilot Projects, RNA Interference.
MESH :
- chemical , genetics : Biomarkers, Tumor, P-Glycoprotein.
- chemical , metabolism : Alanine, Amino Acids, Biomarkers, Tumor, Glucose, Glycerylphosphorylcholine, Lactates, P-Glycoprotein, Phosphatidylethanolamines, Phospholipids.
- genetics : Melanoma.
- metabolism : Cell Membrane, Melanoma, Neoplastic Stem Cells.
- methods : Metabolomics.
- pathology : Melanoma.
- Cell Line, Tumor, Gene Expression Regulation, Neoplastic, Humans, Magnetic Resonance Spectroscopy, Pilot Projects, RNA Interference.

Abstract

We present a pilot study aimed at determining the effects of expression of ATP-binding cassette member B5 (ABCB5), a previously described marker for melanoma-initiating cells, on cellular metabolism. Metabolic profiles for two groups of human G3361 melanoma cells were compared, i.e. wildtype melanoma cells with intact ABCB5 expression (ABCB5-WT) and corresponding melanoma cell variants with inhibited ABCB5 expression, through shRNA-mediated gene knockdown (ABCB5-KD). A comprehensive metabolomic analysis was performed by using proton and phosphorus NMR spectroscopy of cell extracts to examine water-soluble metabolites and lipids. Parametric and non-parametric statistical analysis of absolute and relative metabolite levels yielded significant differences for compounds involved in glucose, amino acid and phospholipid (PL) metabolism. By contrast, energy metabolism was virtually unaffected by ABCB5 expression. The sum of water-soluble metabolites per total protein was 17% higher in ABCB5-WT vs. ABCB5-KD G3361 variants, but no difference was found for the sum of PLs. Enhanced abundance was particularly pronounced for lactate (+ 23%) and alanine (+ 26%), suggesting an increase in glycolysis and potentially glutaminolysis. Increases in PL degradation products, glycerophosphocholine and glycerophosphoethanolamine (+ 85 and 123%, respectively), and redistributions within the PL pool suggested enhanced membrane PL turnover as a consequence of ABCB5 expression. The possibility of glycolysis modulation by an ABCB5-dependent IL1β-mediated mechanism was supported by functional studies employing monoclonal antibody (mAb)-dependent ABCB5 protein inhibition in wildtype G3361 melanoma cells. Our metabolomic results suggest that the underlying biochemical pathways may offer targets for melanoma therapy, potentially in combination with other treatment forms.

DOI: 10.1371/journal.pone.0161803
PubMed: 27560924

Affiliations:

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<front><div type="abstract" xml:lang="en">We present a pilot study aimed at determining the effects of expression of ATP-binding cassette member B5 (ABCB5), a previously described marker for melanoma-initiating cells, on cellular metabolism. Metabolic profiles for two groups of human G3361 melanoma cells were compared, i.e. wildtype melanoma cells with intact ABCB5 expression (ABCB5-WT) and corresponding melanoma cell variants with inhibited ABCB5 expression, through shRNA-mediated gene knockdown (ABCB5-KD). A comprehensive metabolomic analysis was performed by using proton and phosphorus NMR spectroscopy of cell extracts to examine water-soluble metabolites and lipids. Parametric and non-parametric statistical analysis of absolute and relative metabolite levels yielded significant differences for compounds involved in glucose, amino acid and phospholipid (PL) metabolism. By contrast, energy metabolism was virtually unaffected by ABCB5 expression. The sum of water-soluble metabolites per total protein was 17% higher in ABCB5-WT vs. ABCB5-KD G3361 variants, but no difference was found for the sum of PLs. Enhanced abundance was particularly pronounced for lactate (+ 23%) and alanine (+ 26%), suggesting an increase in glycolysis and potentially glutaminolysis. Increases in PL degradation products, glycerophosphocholine and glycerophosphoethanolamine (+ 85 and 123%, respectively), and redistributions within the PL pool suggested enhanced membrane PL turnover as a consequence of ABCB5 expression. The possibility of glycolysis modulation by an ABCB5-dependent IL1β-mediated mechanism was supported by functional studies employing monoclonal antibody (mAb)-dependent ABCB5 protein inhibition in wildtype G3361 melanoma cells. Our metabolomic results suggest that the underlying biochemical pathways may offer targets for melanoma therapy, potentially in combination with other treatment forms.</div>
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<Abstract><AbstractText>We present a pilot study aimed at determining the effects of expression of ATP-binding cassette member B5 (ABCB5), a previously described marker for melanoma-initiating cells, on cellular metabolism. Metabolic profiles for two groups of human G3361 melanoma cells were compared, i.e. wildtype melanoma cells with intact ABCB5 expression (ABCB5-WT) and corresponding melanoma cell variants with inhibited ABCB5 expression, through shRNA-mediated gene knockdown (ABCB5-KD). A comprehensive metabolomic analysis was performed by using proton and phosphorus NMR spectroscopy of cell extracts to examine water-soluble metabolites and lipids. Parametric and non-parametric statistical analysis of absolute and relative metabolite levels yielded significant differences for compounds involved in glucose, amino acid and phospholipid (PL) metabolism. By contrast, energy metabolism was virtually unaffected by ABCB5 expression. The sum of water-soluble metabolites per total protein was 17% higher in ABCB5-WT vs. ABCB5-KD G3361 variants, but no difference was found for the sum of PLs. Enhanced abundance was particularly pronounced for lactate (+ 23%) and alanine (+ 26%), suggesting an increase in glycolysis and potentially glutaminolysis. Increases in PL degradation products, glycerophosphocholine and glycerophosphoethanolamine (+ 85 and 123%, respectively), and redistributions within the PL pool suggested enhanced membrane PL turnover as a consequence of ABCB5 expression. The possibility of glycolysis modulation by an ABCB5-dependent IL1β-mediated mechanism was supported by functional studies employing monoclonal antibody (mAb)-dependent ABCB5 protein inhibition in wildtype G3361 melanoma cells. Our metabolomic results suggest that the underlying biochemical pathways may offer targets for melanoma therapy, potentially in combination with other treatment forms.</AbstractText>
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</AffiliationInfo>
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</AffiliationInfo>
<AffiliationInfo><Affiliation>Harvard Skin Disease Research Center, Department of Dermatology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.</Affiliation>
</AffiliationInfo>
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</AffiliationInfo>
<AffiliationInfo><Affiliation>Singapore Imaging Consortium, Agency for Science, Technology and Research, Singapore.</Affiliation>
</AffiliationInfo>
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<AffiliationInfo><Affiliation>School of Medical Sciences, Edith Cowan University, Joondalup, Western Australia, Australia.</Affiliation>
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<CoiStatement>These authors have declared that no competing interests exist: NWL, PB, BJW, JM and PJC. I have read the journal's policy and the authors of this manuscript have the following competing interests: MHF is a co-inventor of the ABCB5-related US patent 6,846,883 (Gene encoding a multidrug resistance human P-glycoprotein homologue on chromosome 7p15-21 and uses thereof) assigned to Brigham and Women’s Hospital, Boston, MA, and licensed to Ticeba GmbH (Heidelberg, Germany) and Rheacell GmbH & Co. KG (Heidelberg, Germany). MHF serves as a scientific advisor to Ticeba GmbH and Rheacell GmbH & Co. KG. This does not alter our adherence to PLOS ONE policies on sharing data and materials.</CoiStatement>
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	Serveur d'exploration sur les relations entre la France et l'Australie
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Expression of Cell-Surface Marker ABCB5 Causes Characteristic Modifications of Glucose, Amino Acid and Phospholipid Metabolism in the G3361 Melanoma-Initiating Cell Line.

Expression of Cell-Surface Marker ABCB5 Causes Characteristic Modifications of Glucose, Amino Acid and Phospholipid Metabolism in the G3361 Melanoma-Initiating Cell Line.

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