Expression of Peroxisome Proliferator-Activated Receptor-γ in Colon Cancer: Correlation with Histopathological Parameters, Cell Cycle-Related Molecules, and Patients’ Survival

Theocharis, Stamatios; Giaginis, Constantinos; Parasi, Aikaterini; Margeli, Alexandra; Kakisis, John D.; Agapitos, Emmanuel; Kouraklis, Gregorios

doi:10.1007/s10620-007-9794-4

Cited by 44 publications

(42 citation statements)

References 58 publications

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“…No association was found for PPAR-γ positivity with different Dukes' stages, histological grade of differentiation, tumor location, presence of lymph node and liver metastasis, venous invasion, or tumor cell proliferating capacity assessed as Ki-67 overexpression. On the contrary, PPAR-γ expression was statistically significant correlated with the expression of cell cycle-related molecules [58] .…”

Section: Inflammatory Cytokines and Colorectal Cancermentioning

confidence: 81%

Metabolic syndrome and risk of subsequent colorectal cancer

Pais¹,

Silaghi²,

Silaghi³

et al. 2009

WJG

153

145

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The metabolic syndrome and visceral obesity have an increasing prevalence and incidence in the general population. The actual prevalence of the metabolic syndrome is 24% in US population and between 24.6% and 30.9% in Europe. As demonstrated by many clinical trials (NAHANES Ⅲ, INTERHART) the metabolic syndrome is associated with an increased risk of both diabetes and cardiovascular disease. In addition to cardiovascular disease, individual components of the metabolic syndrome have been linked to the development of cancer, particularly to colorectal cancer. Colorectal cancer is an important public health problem; in the year 2000 there was an estimated total of 944 717 incident cases of colorectal cancer diagnosed world-wide. This association is sustained by many epidemiological studies. Recent reports suggest that individuals with metabolic syndrome have a higher risk of colon or rectal cancer. Moreover, the clusters of metabolic syndrome components increase the risk of associated cancer. The physiopathological mechanism that links metabolic syndrome and colorectal cancer is mostly related to abdominal obesity and insulin resistance. Population and experimental studies demonstrated that hyperinsulinemia, elevated C-peptide, elevated body mass index, high levels of insulin growth factor-1, low levels of insulin growth factor binding protein-3, high leptin levels and low adiponectin levels are all involved in carcinogenesis. Understanding the pathological mechanism that links metabolic syndrome and its components to carcinogenesis has a major clinical significance and may have profound health benefits on a number of diseases including cancer, which represents a major cause of mortality and morbidity in our societies.

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Section: Inflammatory Cytokines and Colorectal Cancermentioning

confidence: 81%

Metabolic syndrome and risk of subsequent colorectal cancer

Pais¹,

Silaghi²,

Silaghi³

et al. 2009

WJG

153

145

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“…Effect of rSG, atra and their combination on hct-15 cell proliferation (mean ± Sd). that pparγ is expressed not only in adipose tissue, where it is involved in lipid metabolism (11), but also in a variety of tumors (12). Upon activation by its specific ligands, PPARγ inhibits the growth of tumor cells (13)(14)(15)(16).…”

Section: Discussionmentioning

confidence: 99%

Rosiglitazone and retinoic acid inhibit proliferation and induce apoptosis in the HCT-15 human colorectal cancer cell line

Miao

Liu

et al. 2011

Experimental and Therapeutic Medicine

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Abstract. the aim of this study was to explore the effects of rosiglitazone (rSG) in combination with all-trans retinoic acid (atra) on the proliferation and apoptosis of the hct-15 human colorectal cancer cell line. hct-15 cells were divided into a blank control group, a vehicle control group and experimental groups (rSG only or atra only or rSG plus atra). Growth inhibition was examined using the mtt assay. apoptosis and cell cycle progression were examined by flow cytometry. The expression of cOx-2, mmp-7 and timp-1 was examined by immunocytochemistry. rSG alone inhibited hct-15 cell proliferation in a concentration-and time-dependent manner (P<0.05). The combination of RSG and ATRA exhibited significant synergy (q>1.15). rSG or atra alone effectively increased the proportion of cells in the G0/G1 phase and decreased the proportion of cells in the S phase, thus inducing apoptosis (p<0.05). the combination of rSG and atra resulted in even stronger G1 cell cycle arrest (p<0.05). hct-15 cells expressed cOx-2, mmp-7 and timp-1, with positive expression rates in the control group of 66.79, 73.21 and 64.08%, respectively. after the combined application of rSG and atra, the positive rates significantly declined to only 19.33, 20.58 and 13.13%, respectively (p<0.01). in conclusion, the combination of rSG and atra reduced the expression of cOx-2, mmp-7 and timp-1, caused cell cycle arrest at the G1 phase and induced apoptosis, which resulted in the inhibition of cell proliferation in the hct-15 human colorectal cancer cell line.

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“…Its expression, however, was not correlated with clinicopathological parameters or outcome [1]. Some molecular parameters depend on the localization within the colorectal tract, which I did not expect.…”

mentioning

confidence: 74%

“…In their current report, Theocharis and coworkers analyze the relation of MCM2 and MCM5 with clinicopathology parameters and molecular parameters of cell proliferation and differentiation well established in colon cancer [1]. While they found MCM2 to be consistently associated with clinicopathological parameters, Ki67 and p53, MCM5 was not.…”

mentioning

confidence: 81%