Dietary lipids and adipocytes: potential therapeutic targets in cancers

Kwan, Hiu Yee; Chao, Xiaojuan; Su, Tao; Fu, Xiu‐Qiong; Liu, Bin; Tse, Anfernee Kai-Wing; Wang, Fong; Yu, Zhi‐Ling

doi:10.1016/j.jnutbio.2014.11.001

Cited by 19 publications

(14 citation statements)

References 145 publications

(185 reference statements)

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“…The distribution of its ingredients with sugar limitations can be disadvantageous for hyperproliferative cells and can lead to tumor regression 14 . However, it should be taken under consideration that a long-term abundant supply of lipids may have an additional impact on tumor growth 15 , and especially high fat diets can also promote tumorigenesis, as reported previously 16 17 .…”

mentioning

confidence: 88%

Long-term High Fat Ketogenic Diet Promotes Renal Tumor Growth in a Rat Model of Tuberous Sclerosis

Liśkiewicz

Kasprowska

Wojakowska

et al. 2016

Sci Rep

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Nutritional imbalance underlies many disease processes but can be very beneficial in certain cases; for instance, the antiepileptic action of a high fat and low carbohydrate ketogenic diet. Besides this therapeutic feature it is not clear how this abundant fat supply may affect homeostasis, leading to side effects. A ketogenic diet is used as anti-seizure therapy i.a. in tuberous sclerosis patients, but its impact on concomitant tumor growth is not known. To examine this we have evaluated the growth of renal lesions in Eker rats (Tsc2+/−) subjected to a ketogenic diet for 4, 6 and 8 months. In spite of existing opinions about the anticancer actions of a ketogenic diet, we have shown that this anti-seizure therapy, especially in its long term usage, leads to excessive tumor growth. Prolonged feeding of a ketogenic diet promotes the growth of renal tumors by recruiting ERK1/2 and mTOR which are associated with the accumulation of oleic acid and the overproduction of growth hormone. Simultaneously, we observed that Nrf2, p53 and 8-oxoguanine glycosylase α dependent antitumor mechanisms were launched by the ketogenic diet. However, the pro-cancerous mechanisms finally took the ascendency by boosting tumor growth.

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mentioning

confidence: 88%

Long-term High Fat Ketogenic Diet Promotes Renal Tumor Growth in a Rat Model of Tuberous Sclerosis

Liśkiewicz

Kasprowska

Wojakowska

et al. 2016

Sci Rep

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“…Tur ki ye Kli nik le ri J Med Sci. 2019;39(1): [89][90][91][92][93][94][95][96][97][98][99][100][101][102][103][104][105][106][107] Cyclin D1 ve cMyc hücrelerin büyümesinde ve çoğalmasında etkili genlerin düzenlenmesinde rol oynamaktadır. 6 Vasküler endotelyal büyüme faktörü (VEGF) gibi anjiogenezde rol oynayan faktörlerin upregülasyonu NF-κB yolağı ile düzenlenmektedir.…”

Section: İnflamatuar Durum Nf-κb Ve Kolorektal Kanser İli̇şki̇si̇unclassified

“…Özellikle palmitik asit ve stearik asit kolonositler için potansiyel mutajeniktir ve aşırı araşidonik asit alımı doğrudan kolorektal kanser ile ilişkili olabilir. 95 Spesifik yağ asitlerinden özellikle omega-3 yağ asitleri incelendiğinde veriler diyetsel omega-3 yağ asilerinin karsinogenez gelişiminin ve ilerlemesinin önlenmesinde önemli oldu-ğunu göstermektedir. [96][97][98] Omega-3 yağ asitlerinin karsinogenezi önlemesi ile ilgili birçok mekanizma öne sürülmektedir:…”

Section: Beslenmeni̇n Kolorektal Kanser Oluşumunda Rolüunclassified

Different Mechanisms and the Role of Nutrition in the Formation of Colorectal Cancer

Atabilen¹,

Akbulut²

2019

Turkiye Klinikleri J Med Sci

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anser, ekonomik açıdan gelişmişlik derecesine bakılmaksızın toplumlar üzerinde büyük bir yük oluşturmaktadır. Özellikle günümüzde toplumların yaşlanma sorunuyla karşı karşıya kalmaları ve obezite, fiziksel inaktivite gibi risk faktörleri prevalansındaki artış kanser oluşum hızını artırmaktadır. Global kanser istatistikleri (GLOBOCAN) 2012 yılında dünyada 14,1 milyon yeni kanser vakası ve 8,2 milyon kansere bağlı mortalite oluştuğunu bildirmiştir. 1 Kanserler arasında sıralama yapıldığında

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“…Besides adipose tissue inflammation, obesity also leads to inflammation in other tissues and organs, including pancreas 32 . Again, obesity-induced inflammation of the pancreas may create a micro-environment that is conducive to the development of chronic pancreatitis and cancer 33 . In addition, obesity is often associated with insulin-resistance and frank diabetes mellitus.…”

Section: Risk Factors For Pancreatitis and Pancreatic Cancermentioning

confidence: 99%

Phosphatidylinositol 3-Kinase

Birtolo

Ptasznik

et al. 2016

Pancreas

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Even though a strong association between inflammation and cancer has been widely accepted, the underlying precise molecular mechanisms are still largely unknown. A complex signaling network between tumor and stromal cells is responsible for the infiltration of inflammatory cells into the cancer micro-environment. Tumor stromal cells such as pancreatic stellate cells (PSCs) and immune cells create a microenvironment that protects cancer cells through a complex interaction, ultimately facilitating their local proliferation and their migration to different sites. Furthermore, PSCs have multiple functions related to local immunity, angiogenesis, inflammation and fibrosis. Recently, many studies have shown that members of the phosphoinositol-3-phosphate kinase (PI3K) family are activated in tumor cells, PSCs and tumor infiltrating inflammatory cells to promote cancer growth. Pro-inflammatory cytokines and chemokines secreted by immune cells and fibroblasts within the tumor environment can activate the PI3K pathway both in cancer and inflammatory cells. In this review, we focus on the central role of the PI3K pathway in regulating the cross-talk between immune/stromal cells and cancer cells. Understanding the role of the PI3K pathway in the development of chronic pancreatitis and cancer is crucial for the discovery of novel and efficacious treatment options.

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Dietary lipids and adipocytes: potential therapeutic targets in cancers

Cited by 19 publications

References 145 publications

Long-term High Fat Ketogenic Diet Promotes Renal Tumor Growth in a Rat Model of Tuberous Sclerosis

Long-term High Fat Ketogenic Diet Promotes Renal Tumor Growth in a Rat Model of Tuberous Sclerosis

Different Mechanisms and the Role of Nutrition in the Formation of Colorectal Cancer

Phosphatidylinositol 3-Kinase

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