PPARγ; and Its Ligands: Potential Antitumor Agents in the Digestive System

Shu, Linjing; Huang, Ru; Wu, Songtao; Chen, Zhaozhao; Sun, Ke; Jiang, Yan; Cai, Xiaoxiao

doi:10.2174/1574888x10666150630111618

Cited by 10 publications

(6 citation statements)

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“…4-hydroxy-2-nonenal increase PPAR gene expression and accelerate adiponectin protein degradation in adipocytes [ 65 ]. Peroxisome-proliferator-activated receptors has been also reported to arrest colorectal cancer proliferation [ 66 , 67 ], however it has also been linked to poor outcome in metastatic colorectal cancer (mCRC) [ 68 ]. 4-hydroxy-2-nonenal also upregulates prostaglandin E2 [ 69 ] and cyclooxygenase-2 (COX-2) [ 70 ], two factors associated with high proliferative colorectal cancer [ 71 ].…”

Section: Biologic Performances Of Obesitymentioning

confidence: 99%

Obesity and colorectal cancer: molecular features of adipose tissue

2016

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The huge part of population in developed countries is overweight or obese. Obesity is often determined by body mass index (BMI) but new accurate methods and ratios have recently appeared to measure body fat or fat located in the intestines. Early diagnosis of obesity is crucial since it is considered an increasing colorectal cancer risk factor. On the one hand, colorectal cancer has been strongly associated with lifestyle factors. A diet rich in red and processed meats may increase colorectal cancer risk; however, high-fiber diets (grains, cereals and fruits) have been associated with a decreased risk of colorectal cancer. Other life-style factors associated with obesity that also increase colorectal cancer risk are physical inactivity, smoking and high alcohol intake. Cutting-edge studies reported that high-risk transformation ability of adipose tissue is due to production of different pro-inflammatory cytokines like IL-8, IL-6 or IL-2 and other enzymes like lactate dehydrogenase (LDH) and tumour necrosis factor alpha (TNFα). Furthermore, oxidative stress produces fatty-acid peroxidation whose metabolites possess very high toxicities and mutagenic properties. 4-hydroxy-2-nonenal (4-HNE) is an active compounds that upregulates prostaglandin E2 which is directly associated with high proliferative colorectal cancer. Moreover, 4-HNE deregulates cell proliferation, cell survival, differentiation, autophagy, senescence, apoptosis and necrosis via mitogen-activated protein kinase (MAPK), phosphoinositide 3-kinase (PIK3CA)—AKT and protein kinase C pathways. Other product of lipid peroxidation is malondialdehyde (MDA) being able to regulate insulin through WNT-pathway as well as having demonstrated its mutagenic capability. Accumulation of point mutation enables genomic evolution of colorectal cancer described in the model of Fearon and Vogelstein. In this review, we will summarize different determination methods and techniques to assess a truthfully diagnosis and we will explain some of the capabilities that performs adipocytes as the largest endocrine organ.

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Section: Biologic Performances Of Obesitymentioning

confidence: 99%

Obesity and colorectal cancer: molecular features of adipose tissue

2016

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“…[33][34][35] Some synthetic PPARc ligands, such as rosiglitazone, troglitazone and ciglitazone, inhibit the proliferation of tumour cells and induce tumour cell apoptosis. [36][37][38][39][40] In this study, we found that TNBG-5602 can increase the expression of PPARc at the mRNA and protein levels in vitro and in vivo. Further study found that a PPARc agonist (RSG) can enhance the lipid accumulation of TNBG-5602, while a PPARc inhibitor (T0070907) can reverse the lipid accumulation of TNBG-5602.…”

Section: Discussionmentioning

confidence: 52%

“…It was discovered that overexpression of PPARγ can inhibit cell proliferation and tumour growth, while it is reversed in PPARγ‐silenced cancer cells . Some synthetic PPARγ ligands, such as rosiglitazone, troglitazone and ciglitazone, inhibit the proliferation of tumour cells and induce tumour cell apoptosis …”

Section: Discussionmentioning

confidence: 99%

TNBG-5602, a novel derivative of quinoxaline, inhibits liver cancer growth via upregulating peroxisome proliferator-activated receptor γ in vitro and in vivo

Wan

Zhang

et al. 2019

Journal of Pharmacy and Pharmacology

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Objectives TNBG‐5602 is a newly synthesized compound with an isoquinoline structure. In the present study, we demonstrated the anticancer effect of TNBG‐5602 in in‐vitro and in‐vivo models and investigated its possible anticancer mechanism. Methods The antiproliferation effect of TNBG‐5602 in vitro was evaluated in human liver cancer cell line QGY‐7701. The acute toxicity of TNBG‐5602 was evaluated in mice. The anticancer activity of TNBG‐5602 in vivo was assessed in a xenograft model of human liver cancer cell line QGY‐7701. Key findings The results of CCK‐8 assay showed that TNBG‐5602 can effectively inhibit the proliferation of liver cancer cells in vitro. The acute toxicity test in mice showed that the LD50 of TNBG‐5602 was 172 mg/kg. In a xenograft liver cancer model, TNBG‐5602 could remarkably inhibit the growth of tumours. During in‐vitro and in‐vivo studies, we noted that TNBG‐5602 could induce lipid accumulation in cancer cells and tissues. Further study indicated that the anticancer effect of TNBG‐5602 may be exerted through activating peroxisome proliferator‐activated receptor γ (PPARγ) and downregulating proliferating cell nuclear antigen (PCNA). Conclusions Our results suggested that TNBG‐5602 might exert potent anticancer activity through increasing the expression of PPARγ.

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“…PPARγ is a member of the PPAR family and is expressed in a variety of cancers [129]. Activation of PPARγ regulates the expression of multiple target genes and inhibits the proliferation or migration of tumor cells [130].…”

Section: Discussionmentioning

confidence: 99%

The role and function of PPARγ in bladder cancer

Peng¹,

Wang²,

Cheng³

et al. 2020

J. Cancer

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Peroxisome proliferator-activated receptor gamma (PPARγ), a member of the nuclear receptor superfamily, participates in multiple physiological and pathological processes. Extensive studies have revealed the relationship between PPARγ and various tumors. However, the expression and function of PPARγ in bladder cancer seem to be controversial. It has been demonstrated that PPARγ affects the occurrence and progression of bladder cancer by regulating proliferation, apoptosis, metastasis, and reactive oxygen species (ROS) and lipid metabolism, probably through PPARγ-SIRT1 feedback loops, the PI3K-Akt signaling pathway, and the WNT/β-catenin signaling pathway. Considering the frequent relapses after chemotherapy, some researchers have focused on the relationship between PPARγ and chemotherapy sensitivity in bladder cancer. Moreover, the feasibility of PPARγ ligands as potential therapeutic targets for bladder cancer has been uncovered. Taken together, this review summarizes the relevant literature and our findings to explore the complicated role and function of PPARγ in bladder cancer.

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PPARγ; and Its Ligands: Potential Antitumor Agents in the Digestive System

Cited by 10 publications

References 0 publications

Obesity and colorectal cancer: molecular features of adipose tissue

Obesity and colorectal cancer: molecular features of adipose tissue

TNBG-5602, a novel derivative of quinoxaline, inhibits liver cancer growth via upregulating peroxisome proliferator-activated receptor γ in vitro and in vivo

The role and function of PPARγ in bladder cancer

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