Adipocytokine levels of colon cancer patients before and after treatment

Kosova, Funda; Coşkun, Teoman; Kaya, Yavuz; Kara, Erdal; Z, Ari

doi:10.4149/bll_2013_083

Cited by 16 publications

(8 citation statements)

References 19 publications

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“…However, the correlation between circulating Nampt level and clinical stage in colorectal cancer remains controversial. The serum Nampt level in the malign group (colon carcinoma) was not significantly different from that in the benign group 31 . Another recent study showed that there were no significant correlations between circulating Nampt level and the TNM staging for CRC, although patients with CRC had significantly higher level of serum Nampt than the control group both before and after adjustment for covariates (e.g.…”

Section: Discussionmentioning

confidence: 67%

Regulative Effect of Nampt on Tumor Progression and Cell Viability in Human Colorectal Cancer

Lv¹,

Zhang²,

Zhu³

et al. 2015

J. Cancer

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Colorectal cancer (CRC) is the third most common cancer disease. Here we examined Nampt expression in patients with CRC and the effect of Nampt on cell viability in CRC cells. Nampt protein was overexpressed in colorectal adenoma as well as colorectal carcinoma. The immunoreactive staining of Nampt was negative in the adjacent normal colorectal tissue, weak in colorectal adenoma, and strong in colorectal carcinoma, which may represent tumor progression. Further evaluation of clinical data showed that Nampt expression was not correlated with the clinicopathological characteristics of CRC. Additionally, our in vitro studies demonstrated that Nampt promotes CRC cell viability, whereas the Nampt inhibitor FK866 suppressed CRC cell viability, which was in concordance with the previous studies in other cancer cells. Treatment with Nampt-siRNA reduced the Nampt protein expression resulting in the inhibition of the cell viability of HCT116 and Caco2. Thus, the involvement of Nampt in cell growth indicates that Nampt may play an important role in colorectal tumorigenesis. As a consequence, our results suggest that Nampt may be considered as a progression marker of colorectal tumor and a potentially therapeutic target for the treatment of CRC.

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Section: Discussionmentioning

confidence: 67%

Regulative Effect of Nampt on Tumor Progression and Cell Viability in Human Colorectal Cancer

Lv¹,

Zhang²,

Zhu³

et al. 2015

J. Cancer

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“…Among the 11 studies, one was case-cohort study conducted in USA [31], while the other 10 studies were of case-control design conducted either in Asia [18, 21, 23, 25, 26, 28] or in Europe [24, 27, 29, 32]. Ten of the studies were matched for age and/or gender [18, 21, 23, 24, 26–29, 31, 32] and 6 of them were adjusted for BMI additionally [21, 23, 24, 26, 27, 31].…”

Section: Resultsmentioning

confidence: 99%

Circulating Resistin Levels and Risk of Colorectal Cancer: A Meta-Analysis

Yang

Fan

Luo

et al. 2016

BioMed Research International

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Objectives. Published data on resistin levels in patients with colorectal cancer (CRC) were conflicting and heterogeneous. We conducted a meta-analysis of observational studies to examine the association of circulating resistin levels with carcinogenesis of the CRC. Methods. Potentially eligible studies published up to November 2015 were searched through MEDLINE, EMBASE, Science Citation Index Expanded database, CNKI, and WanFang database. The pooled weighted mean differences (WMDs) with 95% confidence intervals (CIs) calculated by fixed- or random-effect model were used to estimate the effects. Results. A total of 11 studies involving 965 patients were admitted in our meta-analysis. The pooled effects indicated that resistin levels were higher in CRC patients compared to healthy controls (WMD: 1.47 ng/mL; 95% CI: 0.78 to 2.16), with significant heterogeneity across the studies (I 2 = 72%, p < 0.0001). Subgroup analyses and sensitivity analyses revealed that study quality, design, sample type, and resistin assays may account for this heterogeneity. No publication bias was observed. Conclusions. Our meta-analysis suggests that increased circulating resistin levels are associated with greater risk of colorectal cancer. Given the limited number of available studies and significant heterogeneity, larger well-designed randomized studies are warranted.

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“…Insulin, insulin-like growth factor-1 (IGF1), leptin, adiponectin, steroid hormones, and cytokines are some host factors associated with obesity that not only influences the initiation and progression of breast cancer, but also affects its response to therapies [114]. Reports reveal decreased adiponectin in breast and endometrial cancer and vice versa in non-small cell lung cancer, pancreatic, liver, prostate, gastric, renal cell carcinoma, and colon cancer [115,116,117,118]. Wei et al [119] performed a meta-analysis of 107 studies in a random effect model to analyze the levels of circulating adiponectin in cancer patients versus controls.…”

Section: Obesity Adiponectin and Cancer: Interplay Of Bigwigsmentioning

confidence: 99%

Adiponectin, Obesity, and Cancer: Clash of the Bigwigs in Health and Disease

Parida

Siddharth

Sharma

2019

IJMS

190

148

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Adiponectin is one of the most important adipocytokines secreted by adipocytes and is called a “guardian angel adipocytokine” owing to its unique biological functions. Adiponectin inversely correlates with body fat mass and visceral adiposity. Identified independently by four different research groups, adiponectin has multiple names; Acrp30, apM1, GBP28, and AdipoQ. Adiponectin mediates its biological functions via three known receptors, AdipoR1, AdipoR2, and T-cadherin, which are distributed throughout the body. Biological functions of adiponectin are multifold ranging from anti-diabetic, anti-atherogenic, anti-inflammatory to anti-cancer. Lower adiponectin levels have been associated with metabolic syndrome, type 2 diabetes, insulin resistance, cardiovascular diseases, and hypertension. A plethora of experimental evidence supports the role of obesity and increased adiposity in multiple cancers including breast, liver, pancreatic, prostrate, ovarian, and colorectal cancers. Obesity mediates its effect on cancer progression via dysregulation of adipocytokines including increased production of oncogenic adipokine leptin along with decreased production of adiponectin. Multiple studies have shown the protective role of adiponectin in obesity-associated diseases and cancer. Adiponectin modulates multiple signaling pathways to exert its physiological and protective functions. Many studies over the years have shown the beneficial effect of adiponectin in cancer regression and put forth various innovative ways to increase adiponectin levels.

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Adipocytokine levels of colon cancer patients before and after treatment

Cited by 16 publications

References 19 publications

Regulative Effect of Nampt on Tumor Progression and Cell Viability in Human Colorectal Cancer

Regulative Effect of Nampt on Tumor Progression and Cell Viability in Human Colorectal Cancer

Circulating Resistin Levels and Risk of Colorectal Cancer: A Meta-Analysis

Adiponectin, Obesity, and Cancer: Clash of the Bigwigs in Health and Disease

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