Role of Peroxisome Proliferator Activated Receptor-Gamma in Bacillus Calmette-Guérin Bladder Cancer Therapy

Langle, Yanina; Lodillinsky, Catalina; Belgorosky, Denise; Sandes, Eduardo Omar; Eiján, Ana María

doi:10.1016/j.juro.2012.07.109

Cited by 18 publications

(18 citation statements)

References 25 publications

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“…However, the present results were not in accordance with those of a previous report (13). It is generally accepted that PPAR-γ activates the expression of genes such as PTEN, c-myc and P27, which inhibit cancer proliferation, metastasis and invasion (28). It has been reported previously that after PPAR-γ activation, PTEN expression is elevated in colorectal cancers (13), which contributes to phosphatidylino- (13), which contributes to phosphatidylino- (13), which contributes to phosphatidylinositol (3,4,5)-trisphosphate (PIP3) dephosphorylation, inhibiting the activation of PIP3 and PI3K/AKT signaling.…”

Section: Discussioncontrasting

confidence: 99%

“…It has been reported previously that after PPAR-γ activation, PTEN expression is elevated in colorectal cancers (13), which contributes to phosphatidylino- (13), which contributes to phosphatidylino- (13), which contributes to phosphatidylinositol (3,4,5)-trisphosphate (PIP3) dephosphorylation, inhibiting the activation of PIP3 and PI3K/AKT signaling. Therefore, the cell cycle is generally blocked in the G1 stage, inhibiting proliferation and invasion (28). In the present study, however, PTEN expression was decreased, and PPAR-γ was increased in bladder cancer tissue.…”

Section: Discussioncontrasting

confidence: 53%

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Heterogeneity of PTEN and PPAR‑γ in cancer and their prognostic application to bladder cancer

Zhang

Jen

et al. 2019

Exp Ther Med

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Section: Discussioncontrasting

confidence: 99%

Section: Discussioncontrasting

confidence: 53%

Heterogeneity of PTEN and PPAR‑γ in cancer and their prognostic application to bladder cancer

Zhang

Jen

et al. 2019

Exp Ther Med

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“…Bladder cancer is the fourth most common type of cancer found among men in the United States and an important cause of death worldwide [2, 3]. In 2015 alone, the American Cancer Society predicted a total of 74,000 newly diagnosed cases and 16,000 deaths from bladder cancer in the United States [4].…”

Section: Introductionmentioning

confidence: 99%

Deciphering the Roles of Thiazolidinediones and PPARγin Bladder Cancer

et al. 2017

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The use of thiazolidinedione (TZD) therapy in type II diabetic patients has proven useful in the lowering of blood glucose levels. However, recent investigations have shown that there may be potential health concerns associated, including the risk of developing bladder cancer as well as complications in the cardiovasculature. TZDs are ligands for the nuclear receptor PPARγ, and activation causes lipid uptake and insulin sensitization, both of which are critical processes for diabetic patients whose bodies are unable to utilize insulin effectively. Several studies have shown that PPARγ/TZDs decrease IGF-1 levels and, thus, reduce cancer growth in carcinomas such as the pancreas, colon, liver, and prostate. However, other studies have shed light on the potential of the receptor as a biomarker for uroepithelial carcinomas, particularly due to its stimulatory effect on migration of bladder cancer cells. Furthermore, PPARγ may provide the tumor-promoting microenvironment by de novo synthesis of nutrients that are needed for bladder cancer development. In this review, we closely examine the TZD class of drugs and their effects on PPARγ in patient studies along with additional molecular factors that are positive modulators, such as protein phosphatase 5 (PP5), which may have considerable implications for bladder cancer therapy.

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“…For instance, PPARs increase the transcription level of genes for fatty acid oxidation24 and peroxisomal β-oxidation enzymes, which might be important regulators for the homeostasis of the lipid ligands binding to nuclear receptors2526. Many reports suggested PPARs modulation in cancer cells by either agonist or antagonist may be a potential treatment for metabolic diseases and cancer including BCa272829. Among those, the PPARγ pathway is particularly critical for the cancer stem cell properties of ErbB2-positive breast cancer cells3031, and has been reported to inhibit of ErbB activity in human breast cancer cells32.…”

mentioning

confidence: 99%

Simvastatin induces cell cycle arrest and inhibits proliferation of bladder cancer cells via PPARγ signalling pathway

Wang

Cao

Wang

et al. 2016

Sci Rep

109

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Simvastatin is currently one of the most common drugs for old patients with hyperlipidemia, hypercholesterolemia and atherosclerotic diseases by reducing cholesterol level and anti-lipid properties. Importantly, simvastatin has also been reported to have anti-tumor effect, but the underlying mechanism is largely unknown. We collected several human bladder samples and performed microarray. Data analysis suggested bladder cancer (BCa) was significantly associated with fatty acid/lipid metabolism via PPAR signalling pathway. We observed simvastatin did not trigger BCa cell apoptosis, but reduced cell proliferation in a dose- and time-dependent manner, accompanied by PPARγ-activation. Moreover, flow cytometry analysis indicated that simvastatin induced cell cycle arrest at G0/G1 phase, suggested by downregulation of CDK4/6 and Cyclin D1. Furthermore, simvastatin suppressed BCa cell metastasis by inhibiting EMT and affecting AKT/GSK3β. More importantly, we found that the cell cycle arrest at G0/G1 phase and the alterations of CDK4/6 and Cyclin D1 triggered by simvastatin could be recovered by PPARγ-antagonist (GW9662), whereas the treatment of PPARα-antagonist (GW6471) shown no significant effects on the BCa cells. Taken together, our study for the first time revealed that simvastatin inhibited bladder cancer cell proliferation and induced cell cycle arrest at G1/G0 phase via PPARγ signalling pathway.

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Role of Peroxisome Proliferator Activated Receptor-Gamma in Bacillus Calmette-Guérin Bladder Cancer Therapy

Abstract: Results suggest that PPARg is involved in the antitumor action of bacillus Calmette-Guérin. However, exogenous PPARg agonists would not be a favorable therapeutic modality because they can inhibit the tissue remodeling needed for an overall satisfactory bacillus Calmette-Guérin response.

Cited by 18 publications

References 25 publications

Heterogeneity of PTEN and PPAR‑γ in cancer and their prognostic application to bladder cancer

Heterogeneity of PTEN and PPAR‑γ in cancer and their prognostic application to bladder cancer

Deciphering the Roles of Thiazolidinediones and PPARγin Bladder Cancer

Simvastatin induces cell cycle arrest and inhibits proliferation of bladder cancer cells via PPARγ signalling pathway

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