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Prevention of Dietary-Fat-Fueled Ketogenesis Attenuates BRAF V600E Tumor Growth

Lifestyle factors, including diet, play an important role in the survival of cancer patients. However, the molecular mechanisms underlying pathogenic links between diet and particular oncogenic mutations in human cancers remain unclear. We recently reported that the ketone body acetoacetate selectiv... Full description

Journal Title: Cell Metabolism 07 February 2017, Vol.25(2), pp.358-373
Main Author: Xia, Siyuan
Other Authors: Lin, Ruiting , Jin, Lingtao , Zhao, Liang , Kang, Hee-Bum , Pan, Yaozhu , Liu, Shuangping , Qian, Guoqing , Qian, Zhiyu , Konstantakou, Evmorfia , Zhang, Baotong , Dong, Jin-Tang , Chung, Young Rock , Abdel-Wahab, Omar , Merghoub, Taha , Zhou, Lu , Kudchadkar, Ragini R , Lawson, David H , Khoury, Hanna J , Khuri, Fadlo R , Boise, Lawrence H , Lonial, Sagar , Lee, Benjamin H , Pollack, Brian P , Arbiser, Jack L , Fan, Jun , Lei, Qun-Ying , Chen, Jing
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 1550-4131 ; E-ISSN: 1932-7420 ; DOI: 10.1016/j.cmet.2016.12.010
Link: https://www.sciencedirect.com/science/article/pii/S155041311630643X
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recordid: elsevier_sdoi_10_1016_j_cmet_2016_12_010
title: Prevention of Dietary-Fat-Fueled Ketogenesis Attenuates BRAF V600E Tumor Growth
format: Article
creator:
  • Xia, Siyuan
  • Lin, Ruiting
  • Jin, Lingtao
  • Zhao, Liang
  • Kang, Hee-Bum
  • Pan, Yaozhu
  • Liu, Shuangping
  • Qian, Guoqing
  • Qian, Zhiyu
  • Konstantakou, Evmorfia
  • Zhang, Baotong
  • Dong, Jin-Tang
  • Chung, Young Rock
  • Abdel-Wahab, Omar
  • Merghoub, Taha
  • Zhou, Lu
  • Kudchadkar, Ragini R
  • Lawson, David H
  • Khoury, Hanna J
  • Khuri, Fadlo R
  • Boise, Lawrence H
  • Lonial, Sagar
  • Lee, Benjamin H
  • Pollack, Brian P
  • Arbiser, Jack L
  • Fan, Jun
  • Lei, Qun-Ying
  • Chen, Jing
subjects:
  • Braf V600e
  • Ketogenesis
  • Acetoacetate
  • Precision Diet
  • Cancer Therapy
  • Cancer Metabolism
  • Cancer Risk
  • Dietary Fat
  • Cancer Prevention
  • Dehydroacetic Acid
  • Biology
ispartof: Cell Metabolism, 07 February 2017, Vol.25(2), pp.358-373
description: Lifestyle factors, including diet, play an important role in the survival of cancer patients. However, the molecular mechanisms underlying pathogenic links between diet and particular oncogenic mutations in human cancers remain unclear. We recently reported that the ketone body acetoacetate selectively enhances BRAF V600E mutant-dependent MEK1 activation in human cancers. Here we show that a high-fat ketogenic diet increased serum levels of acetoacetate, leading to enhanced tumor growth potential of BRAF V600E-expressing human melanoma cells in xenograft mice. Treatment with hypolipidemic agents to lower circulating acetoacetate levels or an inhibitory homolog of acetoacetate, dehydroacetic acid, to antagonize acetoacetate-BRAF V600E binding attenuated BRAF V600E tumor growth. These findings reveal a signaling basis underlying a pathogenic role of dietary fat in BRAF V600E-expressing melanoma, providing insights into the design of conceptualized “precision diets” that may prevent or delay tumor progression based on an individual’s specific oncogenic mutation profile. Pathogenic links between diets and particular oncogenes remain unknown. Xia et al. demonstrate that a high-fat diet increases circulating acetoacetate that enhances tumor growth potential of BRAF V600E melanoma cells in mice, which informs the design of a “precision diet” to lower cancer risk and development of metabolism-targeted therapies for cancer treatment.
language: eng
source:
identifier: ISSN: 1550-4131 ; E-ISSN: 1932-7420 ; DOI: 10.1016/j.cmet.2016.12.010
fulltext: fulltext
issn:
  • 1550-4131
  • 15504131
  • 1932-7420
  • 19327420
url: Link


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titlePrevention of Dietary-Fat-Fueled Ketogenesis Attenuates BRAF V600E Tumor Growth
creatorXia, Siyuan ; Lin, Ruiting ; Jin, Lingtao ; Zhao, Liang ; Kang, Hee-Bum ; Pan, Yaozhu ; Liu, Shuangping ; Qian, Guoqing ; Qian, Zhiyu ; Konstantakou, Evmorfia ; Zhang, Baotong ; Dong, Jin-Tang ; Chung, Young Rock ; Abdel-Wahab, Omar ; Merghoub, Taha ; Zhou, Lu ; Kudchadkar, Ragini R ; Lawson, David H ; Khoury, Hanna J ; Khuri, Fadlo R ; Boise, Lawrence H ; Lonial, Sagar ; Lee, Benjamin H ; Pollack, Brian P ; Arbiser, Jack L ; Fan, Jun ; Lei, Qun-Ying ; Chen, Jing
ispartofCell Metabolism, 07 February 2017, Vol.25(2), pp.358-373
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subjectBraf V600e ; Ketogenesis ; Acetoacetate ; Precision Diet ; Cancer Therapy ; Cancer Metabolism ; Cancer Risk ; Dietary Fat ; Cancer Prevention ; Dehydroacetic Acid ; Biology
descriptionLifestyle factors, including diet, play an important role in the survival of cancer patients. However, the molecular mechanisms underlying pathogenic links between diet and particular oncogenic mutations in human cancers remain unclear. We recently reported that the ketone body acetoacetate selectively enhances BRAF V600E mutant-dependent MEK1 activation in human cancers. Here we show that a high-fat ketogenic diet increased serum levels of acetoacetate, leading to enhanced tumor growth potential of BRAF V600E-expressing human melanoma cells in xenograft mice. Treatment with hypolipidemic agents to lower circulating acetoacetate levels or an inhibitory homolog of acetoacetate, dehydroacetic acid, to antagonize acetoacetate-BRAF V600E binding attenuated BRAF V600E tumor growth. These findings reveal a signaling basis underlying a pathogenic role of dietary fat in BRAF V600E-expressing melanoma, providing insights into the design of conceptualized “precision diets” that may prevent or delay tumor progression based on an individual’s specific oncogenic mutation profile. Pathogenic links between diets and particular oncogenes remain unknown. Xia et al. demonstrate that a high-fat diet increases circulating acetoacetate that enhances tumor growth potential of BRAF V600E melanoma cells in mice, which informs the design of a “precision diet” to lower cancer risk and development of metabolism-targeted therapies for cancer treatment.
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titlePrevention of Dietary-Fat-Fueled Ketogenesis Attenuates BRAF V600E Tumor Growth
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Lifestyle factors, including diet, play an important role in the survival of cancer patients. However, the molecular mechanisms underlying pathogenic links between diet and particular oncogenic mutations in human cancers remain unclear. We recently reported that the ketone body acetoacetate selectively enhances BRAF V600E mutant-dependent MEK1 activation in human cancers. Here we show that a high-fat ketogenic diet increased serum levels of acetoacetate, leading to enhanced tumor growth potential of BRAF V600E-expressing human melanoma cells in xenograft mice. Treatment with hypolipidemic agents to lower circulating acetoacetate levels or an inhibitory homolog of acetoacetate, dehydroacetic acid, to antagonize acetoacetate-BRAF V600E binding attenuated BRAF V600E tumor growth. These findings reveal a signaling basis underlying a pathogenic role of dietary fat in BRAF V600E-expressing melanoma, providing insights into the design of conceptualized “precision diets” that may prevent or delay tumor progression based on an individual’s specific oncogenic mutation profile.

Pathogenic links between diets and particular oncogenes remain unknown. Xia et al. demonstrate that a high-fat diet increases circulating acetoacetate that enhances tumor growth potential of BRAF V600E melanoma cells in mice, which informs the design of a “precision diet” to lower cancer risk and development of metabolism-targeted therapies for cancer treatment.

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abstract

Lifestyle factors, including diet, play an important role in the survival of cancer patients. However, the molecular mechanisms underlying pathogenic links between diet and particular oncogenic mutations in human cancers remain unclear. We recently reported that the ketone body acetoacetate selectively enhances BRAF V600E mutant-dependent MEK1 activation in human cancers. Here we show that a high-fat ketogenic diet increased serum levels of acetoacetate, leading to enhanced tumor growth potential of BRAF V600E-expressing human melanoma cells in xenograft mice. Treatment with hypolipidemic agents to lower circulating acetoacetate levels or an inhibitory homolog of acetoacetate, dehydroacetic acid, to antagonize acetoacetate-BRAF V600E binding attenuated BRAF V600E tumor growth. These findings reveal a signaling basis underlying a pathogenic role of dietary fat in BRAF V600E-expressing melanoma, providing insights into the design of conceptualized “precision diets” that may prevent or delay tumor progression based on an individual’s specific oncogenic mutation profile.

Pathogenic links between diets and particular oncogenes remain unknown. Xia et al. demonstrate that a high-fat diet increases circulating acetoacetate that enhances tumor growth potential of BRAF V600E melanoma cells in mice, which informs the design of a “precision diet” to lower cancer risk and development of metabolism-targeted therapies for cancer treatment.

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