ArticleMolecular metabolism2015
High-calorie diet exacerbates prostate neoplasia in mice with haploinsufficiency of Pten tumor suppressor gene.
Article in Molecular metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- Exploring the role of metabolic disorders and gut microbiome in immune checkpoint regulation in cancer: PI3K/AKT/mTOR focus.Journal of physiology and biochemistry · 2026Review
- Carcinoembryonic antigen-related cell adhesion molecule 1 in cancer: Blessing or curse?European journal of clinical investigation · 2024Review
- Metabolic adaptations in prostate cancer.British journal of cancer · 2024Review
- The Effects of High Fat Diet on the Incidence of Obesity and Monocyte Chemoattractant Protein-1 Levels on Histological Changes in Prostate Wistar Rats.Research and reports in urology · 2024Article
- Grape Powder Supplementation Attenuates Prostate Neoplasia Associated with Pten Haploinsufficiency in Mice Fed High-Fat Diet.Molecular nutrition & food research · 2020Article
- Loss of Ceacam1 promotes prostate cancer progression in Pten haploinsufficient male mice.Metabolism: clinical and experimental · 2020Article
- PTEN: A Thrifty Gene That Causes Disease in Times of Plenty?Frontiers in nutrition · 2020Article
- High-fat diet fuels prostate cancer progression by rewiring the metabolome and amplifying the MYC program.Nature communications · 2019Article
- Dietary palmitate cooperates with Src kinase to promote prostate tumor progression.The Prostate · 2019Article
- Research Evidence on High-Fat Diet-Induced Prostate Cancer Development and Progression.Journal of clinical medicine · 2019Review
- Metabolic Vulnerabilities of Prostate Cancer: Diagnostic and Therapeutic Opportunities.Cold Spring Harbor perspectives in medicine · 2018Review
- Obesity does not promote tumorigenesis of localized patient-derived prostate cancer xenografts.Oncotarget · 2016Article
- Effect of body mass index on the performance characteristics of PSA-related markers to detect prostate cancer.Scientific reports · 2016Article
- Obesity and cancer: mechanistic insights from transdisciplinary studies.Endocrine-related cancer · 2015Review
- Linking obesogenic dysregulation to prostate cancer progression.Endocrine connections · 2015Review
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
Abstract
objectiveAssociation between prostate cancer and obesity remains controversial. Allelic deletions of PTEN, a tumor suppressor gene, are common in prostate cancer in men. Monoallelic Pten deletion in mice causes low prostatic intraepithelial neoplasia (mPIN). This study tested the effect of a hypercaloric diet on prostate cancer in Pten (+/-) mice.
methods1-month old mice were fed a high-calorie diet deriving 45% calories from fat for 3 and 6 months before prostate was analyzed histologically and biochemically for mPIN progression. Because Pten (+/-) mice are protected against diet-induced insulin resistance, we tested the role of insulin on cell growth in RWPE-1 normal human prostatic epithelial cells with siRNA knockdown of PTEN.
resultsIn addition to activating PI3 kinase/Akt and Ras/MAPkinase pathways, high-calorie diet causes neoplastic progression, angiogenesis, inflammation and epithelial-mesenchymal transition. It also elevates the expression of fatty acid synthase (FAS), a lipogenic gene commonly elevated in progressive cancer. SiRNA-mediated downregulation of PTEN demonstrates increased cell growth and motility, and soft agar clonicity in addition to elevation in FAS in response to insulin in RWPE-1 normal human prostatic cells. Downregulating FAS in addition to PTEN, blunted the proliferative effect of insulin (and IL-6) in RWPE-1 cells.
conclusionHigh-calorie diet promotes prostate cancer progression in the genetically susceptible Pten haploinsufficient mouse while preserving insulin sensitivity. This appears to be partly due to increased inflammatory response to high-caloric intake in addition to increased ability of insulin to promote lipogenesis.
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