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Effect of PTEN loss on metabolic reprogramming in prostate cancer cells

The tumor suppressor gene PTEN is one of the most often deleted genes in human prostate cancer. Loss of PTEN is an important event in prostate carcinogenesis. Metabolic reprogramming induced by PTEN loss fuels malignant growth and proliferation of prostate cancer cells. Targeted metabolomics analysi...

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Autores principales: Zhou, Xin, Yang, Xu, Sun, Xiang, Xu, Xinyuan, Li, Xi'an, Guo, Yan, Wang, Jiancai, Li, Xia, Yao, Libo, Wang, He, Shen, Lan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6386093/
https://www.ncbi.nlm.nih.gov/pubmed/30854061
http://dx.doi.org/10.3892/ol.2019.9932
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author Zhou, Xin
Yang, Xu
Sun, Xiang
Xu, Xinyuan
Li, Xi'an
Guo, Yan
Wang, Jiancai
Li, Xia
Yao, Libo
Wang, He
Shen, Lan
author_facet Zhou, Xin
Yang, Xu
Sun, Xiang
Xu, Xinyuan
Li, Xi'an
Guo, Yan
Wang, Jiancai
Li, Xia
Yao, Libo
Wang, He
Shen, Lan
author_sort Zhou, Xin
collection PubMed
description The tumor suppressor gene PTEN is one of the most often deleted genes in human prostate cancer. Loss of PTEN is an important event in prostate carcinogenesis. Metabolic reprogramming induced by PTEN loss fuels malignant growth and proliferation of prostate cancer cells. Targeted metabolomics analysis was used to investigate the effects of PTEN loss on intracellular metabolic pathways in prostate cancer cells. DU-145 cells were transfected with PTEN siRNAs (siRNA-1 and siRNA-2) for 48 h, and endogenous PTEN expression was monitored by western blotting. Changes in intracellular metabolites were determined by liquid chromatography-tandem mass chromatography (LC-MS/MS) and gas chromatography-mass spectrometry (GC-MS). Most intracellular metabolites involved in glycolysis and glutaminolysis were increased in PTEN knockdown prostate cancer cells. In addition, most intracellular metabolites involved in fatty acid de novo synthesis, fatty acid beta oxidation and branched chain amino acid catabolism were also increased in PTEN knockdown prostate cancer cells. These results revealed that PTEN loss induced the metabolic reprogramming of prostate cancer cells and promoted the malignant proliferation of prostate cancer cells. The present metabolomics analysis indicates that tumor suppressor gene PTEN mutation or deletion can induce metabolic reprogramming in prostate cancer cells and tumorigenesis by altering the metabolic flux of glycolysis, glutaminolysis, fatty acid metabolism and branched chain amino acid catabolism pathways. Metabolic reprogramming is one of the contributors to PTEN-loss driven prostate cancer.
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spelling pubmed-63860932019-03-08 Effect of PTEN loss on metabolic reprogramming in prostate cancer cells Zhou, Xin Yang, Xu Sun, Xiang Xu, Xinyuan Li, Xi'an Guo, Yan Wang, Jiancai Li, Xia Yao, Libo Wang, He Shen, Lan Oncol Lett Articles The tumor suppressor gene PTEN is one of the most often deleted genes in human prostate cancer. Loss of PTEN is an important event in prostate carcinogenesis. Metabolic reprogramming induced by PTEN loss fuels malignant growth and proliferation of prostate cancer cells. Targeted metabolomics analysis was used to investigate the effects of PTEN loss on intracellular metabolic pathways in prostate cancer cells. DU-145 cells were transfected with PTEN siRNAs (siRNA-1 and siRNA-2) for 48 h, and endogenous PTEN expression was monitored by western blotting. Changes in intracellular metabolites were determined by liquid chromatography-tandem mass chromatography (LC-MS/MS) and gas chromatography-mass spectrometry (GC-MS). Most intracellular metabolites involved in glycolysis and glutaminolysis were increased in PTEN knockdown prostate cancer cells. In addition, most intracellular metabolites involved in fatty acid de novo synthesis, fatty acid beta oxidation and branched chain amino acid catabolism were also increased in PTEN knockdown prostate cancer cells. These results revealed that PTEN loss induced the metabolic reprogramming of prostate cancer cells and promoted the malignant proliferation of prostate cancer cells. The present metabolomics analysis indicates that tumor suppressor gene PTEN mutation or deletion can induce metabolic reprogramming in prostate cancer cells and tumorigenesis by altering the metabolic flux of glycolysis, glutaminolysis, fatty acid metabolism and branched chain amino acid catabolism pathways. Metabolic reprogramming is one of the contributors to PTEN-loss driven prostate cancer. D.A. Spandidos 2019-03 2019-01-14 /pmc/articles/PMC6386093/ /pubmed/30854061 http://dx.doi.org/10.3892/ol.2019.9932 Text en Copyright: © Zhou et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Zhou, Xin
Yang, Xu
Sun, Xiang
Xu, Xinyuan
Li, Xi'an
Guo, Yan
Wang, Jiancai
Li, Xia
Yao, Libo
Wang, He
Shen, Lan
Effect of PTEN loss on metabolic reprogramming in prostate cancer cells
title Effect of PTEN loss on metabolic reprogramming in prostate cancer cells
title_full Effect of PTEN loss on metabolic reprogramming in prostate cancer cells
title_fullStr Effect of PTEN loss on metabolic reprogramming in prostate cancer cells
title_full_unstemmed Effect of PTEN loss on metabolic reprogramming in prostate cancer cells
title_short Effect of PTEN loss on metabolic reprogramming in prostate cancer cells
title_sort effect of pten loss on metabolic reprogramming in prostate cancer cells
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6386093/
https://www.ncbi.nlm.nih.gov/pubmed/30854061
http://dx.doi.org/10.3892/ol.2019.9932
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