Adiponectin deficiency: Role in chronic inflammation induced colon cancer

Saxena, Arpit; Chumanevich, Alexander A.; Fletcher, Emma; Larsen, Bianca; Lattwein, Kirby; Kaur, Kirandeep; Fayad, Raja

doi:10.1016/j.bbadis.2011.12.006

Cited by 69 publications

(52 citation statements)

References 47 publications

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“…At least in this model, higher adiponectin levels had no effect on colon tumor incidence, number, or size. This finding is in contrast to results recently published by Saxena et al [43]. They used a different model, i.e.…”

Section: Adipocytokines and Their Role In Hcccontrasting

confidence: 56%

Adipocytokines and Hepatocellular Carcinoma

Wieser

Moschen²,

Tilg³

2012

Dig Dis

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Adipocytokines are primarily adipocyte-derived products, although certain members are also synthesized by other cell types. These adipocytokines, similarly to classical cytokines, are characterized by very pleiotropic functions affecting biological processes throughout the body. An increasing number of adipocytokines has recently been recognized, such as adiponectin, leptin, pre-B cell colony-enhancing factor/Nampt/visfatin, resistin, progranulin, and others. Adiponectin has emerged as the most abundant circulating adipocytokine, is produced almost exclusively by adipocytes, and has mainly anti-inflammatory and anti-diabetic functions. In contrast, leptin is produced by many cell types beyond adipocytes, regulates immunity and T cell functions, and acts in a more pro-inflammatory fashion. Adipocytokines play a fundamental role in adipose tissue homeostasis (i.e. health) and disease, especially in obesity-related disorders such as non-alcoholic fatty liver diseases (NAFLD) and their complications, including hepatocellular carcinoma (HCC). Lack of adiponectin as observed in NAFLD drives steatosis and inflammation in the liver, and evidence is increasing that this adipocytokine has many anti-tumor properties and might play a rather protective role in HCC. The role of leptin in NAFLD is still unclear and this adipocytokine seems to have opposite effects in HCC, acting more as a tumor promoter. Evidence is increasing that HCC tissue produces various adipocytokines, and adiponectin expression in HCC seems to be decreased whereas leptin expression is rather increased. In conclusion, adipocytokines are increasingly recognized as pleiotropic molecules involved in the pathophysiology of HCC, which might lead to therapeutic approaches targeting these mediators.

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Section: Adipocytokines and Their Role In Hcccontrasting

confidence: 56%

Adipocytokines and Hepatocellular Carcinoma

Wieser

Moschen²,

Tilg³

2012

Dig Dis

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“…Thus, APN has a proinflammatory role in colitis and anti-inflammatory effects in atherosclerosis (12). However, another group reported that in a chronic inflammation-induced colon cancer model, APNKO mice had higher levels of immune cell infiltration and inflammation than did wild-type (WT) mice (13). Until now, there have been discrepancies regarding the role of APN in inflammation and tumor models.…”

mentioning

confidence: 96%

Adiponectin Deficiency Suppresses Lymphoma Growth in Mice by Modulating NK Cells, CD8 T Cells, and Myeloid-Derived Suppressor Cells

Han

Jeong

Lee

et al. 2013

The Journal of Immunology

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Previously, we found that adiponectin (APN) suppresses IL-2–induced NK cell activation by downregulating the expression of the IFN-γ–inducible TNF-related apoptosis-inducing ligand and Fas ligand. Although the antitumor function of APN has been reported in several types of solid tumors, with few controversial results, no lymphoma studies have been conducted. In this study, we assessed the role of APN in immune cell function, including NK cells, CTLs, and myeloid-derived suppressor cells, in EL4 and B16F10 tumor-bearing APN knockout (KO) mice. We observed attenuated EL4 growth in the APNKO mice. Increased numbers of splenic NK cells and splenic CTLs were identified under naive conditions and EL4-challenged conditions, respectively. In APNKO mice, splenic NK cells showed enhanced cytotoxicity with and without IL-2 stimulation. Additionally, there were decreased levels of myeloid-derived suppressor cell accumulation in the EL4-bearing APNKO mice. Enforced MHC class I expression on B16F10 cells led to attenuated growth of these tumors in APNKO mice. Thus, our results suggest that EL4 regression in APNKO mice is not only due to an enhanced antitumor immune response but also to a high level of MHC class I expression.

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“…APN deficiency induces chronic inflammation of the large intestine, which may further develop into CRC and increase the risk of developing cancer. Saxena et al (31) have investigated DMH-induced CRC under the condition of APN deficiency and identified that experimental animals deficient in APN clearly exhibit the clinical symptoms of carcinogenesis.…”

Section: A B C D E Fmentioning

confidence: 99%

Effects of high-fat diet on 1,2-dimethylhydrazine-induced aberrant crypt foci and colorectal tumours in rats

Qi¹,

Tang²,

Zhou³

et al. 2015

Biomedical Reports

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Abstract. Obesity is one of the leading causes of numerous types of cancer. The present study investigated the impact of a high-fat diet on 1,2-dimethylhydrazine (DMH)-induced colorectal cancer (CRC) in F344 rats. A total of 16 male F344 rats aged 4 weeks were randomly divided into two groups (8 rats/group). Rats in group A were fed a basal diet with a moderate fat (MF) content, while rats in group B were fed a high-fat diet. Upon reaching 5 weeks of age, the rats were injected subcutaneously with DMH (20 mg/kg body weight). DMH was administered once a week for 8 consecutive weeks. All the rats were sacrificed 34 weeks after the first DMH injection and dissected to obtain samples of colorectal tissues. The tissues were examined under a microscope for the presence of aberrant crypt foci (ACFs) and subjected to histopathological analysis. The results showed that at the end of the 34-week experiment, body weights and visceral fat levels were significantly higher in the high-fat diet group compared to the basal diet group. In addition, the incidences of colorectal ACF, adenoma and adenocarcinoma were markedly elevated in the high-fat diet group compared to the basal diet group. These results indicate that the consumption of a high-fat diet promotes the development and progression of CRC and the control of fat intake may prevent CRC.

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Adiponectin deficiency: Role in chronic inflammation induced colon cancer

Cited by 69 publications

References 47 publications

Adipocytokines and Hepatocellular Carcinoma

Adipocytokines and Hepatocellular Carcinoma

Adiponectin Deficiency Suppresses Lymphoma Growth in Mice by Modulating NK Cells, CD8 T Cells, and Myeloid-Derived Suppressor Cells

Effects of high-fat diet on 1,2-dimethylhydrazine-induced aberrant crypt foci and colorectal tumours in rats

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