scholarly journals Metformin inhibits prostate cancer growth induced by a high‐fat diet inPten‐deficient model mice

2018 ◽  
Vol 26 (2) ◽  
pp. 307-309 ◽  
Author(s):  
Takuji Hayashi ◽  
Kazutoshi Fujita ◽  
Makoto Matsushita ◽  
Yujiro Hayashi ◽  
Motohide Uemura ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
High Fat Diet ◽  
Cancer Growth ◽  
High Fat

scholarly journals Signal transducer and activator of transcription-3 drives the high-fat diet-associated prostate cancer growth

2019 ◽  
Vol 10 (9) ◽  
Author(s):  
Hiu Yee Kwan ◽  
Bin Liu ◽  
Chunhua Huang ◽  
Sarwat Fatima ◽  
Tao Su ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
High Fat Diet ◽  
Cancer Growth ◽  
Signal Transducer ◽  
High Fat ◽  
Transcription 3

scholarly journals High-Fat Diet-Induced Inflammation Accelerates Prostate Cancer Growth via IL6 Signaling

2018 ◽  
Vol 24 (17) ◽  
pp. 4309-4318 ◽  
Author(s):  
Takuji Hayashi ◽  
Kazutoshi Fujita ◽  
Satoshi Nojima ◽  
Yujiro Hayashi ◽  
Kosuke Nakano ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
High Fat Diet ◽  
Cancer Growth ◽  
High Fat

244 MiR-130a modulates high-fat diet-induced tumour progression through the activation of MET in prostate cancer

2016 ◽  
Vol 15 (3) ◽  
pp. e244
Author(s):  
S. Narita ◽  
Y. Matsuda ◽  
T. Nara ◽  
M. Huang ◽  
T. Yoshioka ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
High Fat Diet ◽  
Tumour Progression ◽  
High Fat

Abstract 2674: High fat diet accelerates MYC-driven prostate cancer through metabolic and epigenomic rewiring

2016 ◽  
Author(s):  
David P. Labbe’ ◽  
Giorgia Zadra ◽  
Meng Yang ◽  
Charles Y. Lin ◽  
Jaime M. Reyes ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
High Fat Diet ◽  
High Fat

Abstract B39: PTP1B deficiency potentiate prostate cancer invasiveness by sensitizing Pten-null tumors to high-fat diet

2016 ◽  
Author(s):  
David P. Labbé ◽  
Noriko Uetani ◽  
Valérie Vinette ◽  
Isabelle Aubry ◽  
Eva Migon ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
High Fat Diet ◽  
High Fat ◽  
Cancer Invasiveness

scholarly journals Toll-like receptor 4 is a master regulator for colorectal cancer growth under high-fat diet by programming cancer metabolism

2021 ◽  
Vol 12 (8) ◽  
Author(s):  
Xianjing Hu ◽  
Sarwat Fatima ◽  
Minting Chen ◽  
Keyang Xu ◽  
Chunhua Huang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Palmitic Acid ◽  
High Fat Diet ◽  
Cancer Metabolism ◽  
Cancer Growth ◽  
Dependent Manner ◽  
Tlr4 Expression ◽  
High Fat ◽  
Master Regulator ◽  
Tumor Tissues

AbstractAlthough high-fat diet (HFD) has been implicated in the development of colorectal cancer (CRC), the critical signaling molecule that mediates the cancer growth is not well-defined. Identifying the master regulator that controls CRC growth under HFD can facilitate the development of effective therapeutics for the cancer treatment. In this study, the global lipidomics and RNA sequencing data show that, in the tumor tissues of CRC-bearing mouse models, HFD not only increases tumor weight, but also the palmitic acid level and TLR4 expression, which are reduced when HFD is replaced by control diet. These concomitant changes suggest the roles of palmitic acid and TLR4 in CRC growth. Subsequent studies show that palmitic acid regulates TLR4 expression in PU.1-dependent manner. Knockdown of PU.1 or mutations of PU.1-binding site on TLR4 promoter abolish the palmitic acid-increased TLR4 expression. The role of palmitic acid/PU.1/TLR4 axis in CRC growth is further examined in cell model and animal models that are fed either HFD or palmitic acid-rich diet. More importantly, iTRAQ proteomics data show that knockdown of TLR4 changes the metabolic enzyme profiles in the tumor tissues, which completely abolish the HFD-enhanced ATP production and cancer growth. Our data clearly demonstrate that TLR4 is a master regulator for CRC growth under HFD by programming cancer metabolism.

143 HIGH-FAT DIET INCREASES RENAL CANCER GROWTH ACCOMPANIED BY LEPTIN INCREASE, AND SURVIVIN INHIBITION IS EFFECTIVE FOR SIMVASTATIN RESISTANT RENAL CANCER

2012 ◽  
Vol 187 (4S) ◽  
Author(s):  
Hidekazu Koike ◽  
Takashi Nitta ◽  
Yoshitaka Sekine ◽  
Yosuke Furuya ◽  
Yasuyuki Morikawa ◽  
...  
Keyword(s):  
Renal Cancer ◽  
High Fat Diet ◽  
Cancer Growth ◽  
High Fat

scholarly journals Macrophage Inhibitory Cytokine-1 Induced by a High-Fat Diet Promotes Prostate Cancer Progression by Stimulating Tumor Promoting Cytokine Production from Tumor Stromal Cells

2020 ◽  
Author(s):  
Mingguo Huang ◽  
Shintaro Narita ◽  
Atsushi Koizumi ◽  
Taketoshi Nara ◽  
Kazuyuki Numakura ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Progression ◽  
High Fat Diet ◽  
Control Diet ◽  
High Body Mass Index ◽  
High Serum ◽  
High Fat ◽  
Stromal Fibroblasts ◽  
Stromal Microenvironment

Abstract Background: Recent studies have indicated that a high-fat diet (HFD) and/or HFD-induced obesity may influence prostate cancer (PCa) progression, but the role of HFD in PCa microenvironment is unclear. Methods: In this study, we investigated the role of HFD on PCa stromal microenvironment using the PC-3M-luc-C6 PCa model mice fed with HFD or control diet, especially focusing on macrophage inhibitory cytokine-1 (MIC-1) and its effect on the tumor microenvironment. In addition, the synergistic effect of periprostatic adipocytes (PPAC), derived from primary PCa patients, on activation and cytokine secretion of prostate stromal fibroblasts were investigated. The expression pattern and role of MIC-1 signaling on human PCa stroma activation and PCa progression were investigated.Results: The HFD consumption stimulated PCa cell growth and invasion as a result of upregulated MIC-1 signaling and subsequent increased secretion of interleukin (IL)-8 and IL-6 from prostate stromal fibroblasts in the PC-3M-luc-C6 PCa model mice. In addition, PPAC directly stimulated MIC-1 production from PC-3 cells and IL-8 secretion in prostate stromal fibroblasts through upregulation of the adipolysis and free fatty acid (FFA) release. The increased serum MIC-1 was significantly correlated with human PCa stroma activation, high serum IL-8, IL-6 and lipase activity, advanced PCa progression, and high body mass index of the patients. Glial-derived neurotrophic factor receptor alpha-like (GFRAL), a specific receptor of MIC-1, was highly expressed in both the cytoplasm and membrane of the PCa cells and the surrounding stromal fibroblasts, and the expression level was decreased by androgen deprivation therapy and chemotherapy. Conclusion: HFD-mediated activation of the PCa stromal microenvironment through metabolically upregulated MIC-1 signaling by increased available free fatty acids may be a critical mechanism of HFD and/or obesity induced PCa progression.

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