Ligands for the peroxisome proliferator-activated receptor-γ have inhibitory effects on growth of human neuroblastoma cells in vitro

Valentiner, Ursula; Carlsson, Margarita; Erttmann, R.; Hildebrandt, Herbert; Schumacher, Udo

doi:10.1016/j.tox.2005.05.024

Cited by 32 publications

(26 citation statements)

References 40 publications

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“…Although rosiglitazone is the most potent and selective synthetic ligand of PPARγ, it suppresses cancer cell growth through PPARγ-dependent and independent [22] signal path ways, because different cellular models may be, at least in part, responsible for the discrepancies. In the present study, rosiglitazone increased PPARγ expression in a time-dependent manner.…”

Section: Discussionmentioning

confidence: 99%

Rosiglitazone enhances fluorouracil-induced apoptosis of HT-29 cells by activating peroxisome proliferator-activated receptor γ

Zhang

Tang²,

Sun³

et al. 2007

WJG

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Section: Discussionmentioning

confidence: 99%

Rosiglitazone enhances fluorouracil-induced apoptosis of HT-29 cells by activating peroxisome proliferator-activated receptor γ

Zhang

Tang²,

Sun³

et al. 2007

WJG

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“…In addition, it might be hypothesised that PPARg overexpression in transfected SH-SY5Y cells might increase the level of unphosphorylated PPARg beyond a critical threshold, thus eliciting transcriptional activity. Other recent studies have shown variable antineoplastic effects of PPARg agonists in NB cell lines expressing PPARg (Han et al, 2001, Servidei et al, 2004, Valentiner et al, 2005, but the activity of PPARg was addressed only in one study, in which PPARg was found to be functionally active in different cell lines and particularly in SK-N-AS (Servidei et al, 2004). However, the relationship between PPARg transactivation and the response to TZDs was not addressed.…”

Section: Discussionmentioning

confidence: 99%

“…The aim of our study was to evaluate the role of the PPARg agonist rosiglitazone (RGZ) on cell growth, adhesion, invasiveness and apoptosis in two different NB cell lines (SK-N-AS and SH-SY5Y), which express PPARg (Servidei et al, 2004, Valentiner et al, 2005. Furthermore, transient transfection experiments with a peroxisome proliferator response element-luciferase reporter plasmid were performed, in order to determine whether cell response to RGZ was related to the level of PPARg transcriptional activity.…”

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confidence: 99%

Antineoplastic effects of rosiglitazone and PPARγ transactivation in neuroblastoma cells

et al. 2006

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Neuroblastoma (NB) is the most common extracranial solid tumour in infants. Unfortunately, most children present with advanced disease and have a poor prognosis. In the present study, we evaluated the role of the peroxisome proliferator-activated receptor γ (PPAR γ ) agonist rosiglitazone (RGZ) in two NB cell lines (SK-N-AS and SH-SY5Y), which express PPAR γ . Rosiglitazone decreased cell proliferation and viability to a greater extent in SK-N-AS than in SH-SY5Y. Furthermore, 20 μ M RGZ significantly inhibited cell adhesion, invasiveness and apoptosis in SK-N-AS, but not in SH-SY5Y. Because of the different response of SK-N-AS and SH-SY5Y cells to RGZ, the function of PPAR γ as a transcriptional activator was assessed. Noticeably, transient transcription experiments with a PPAR γ responsive element showed that RGZ induced a three-fold increase of the reporter activity in SK-N-AS, whereas no effect was observed in SH-SY5Y. The different PPAR γ activity may be likely due to the markedly lower amount of phopshorylated (i.e. inactive) protein observed in SK-N-AS. To our knowledge, this is the first demonstration that the differential response of NB cells to RGZ may be related to differences in PPAR γ transactivation. This finding indicates that PPAR γ activity may be useful to select those patients, for whom PPAR γ agonists may have a beneficial therapeutic effect.

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“…Rosiglitazone was found to maximally inhibit the growth of H295R cells at the dose of 10 lM, 14 whereas in some neuroblastoma cells, 100 lM of rosiglitazone was needed to reach a maximal growth inhibition. 15 A low dose of rosiglitazone ( 30 lM) had no inhibitory effect on HT-29 cell proliferation, but an even lower dose (10 lM) could sensitize HT-29 cells to 5-FUinduced apoptosis. 16 Contradictory to this study, treatment of HT-29 cells with 0-10 lM of rosiglitazone resulted in a dose-and time-dependent inhibition of cell growth and apoptosis.…”

mentioning

confidence: 96%

“…Rosiglitazone has been tested on various cancers including colon cancer [14][15][16][17][18][19][20] with wide effective dose ranges. However, the anticancer effect of rosiglitazone varies considerably in different cancers, and even in the same cancer type, the reported results are variable.…”

mentioning

confidence: 99%

Loss of XIAP sensitizes rosiglitazone‐induced growth inhibition of colon cancer in vivo

Dai

Qiao

Chan

et al. 2008

Intl Journal of Cancer

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Ligands for peroxisome proliferator-activated receptor gamma (PPARc) possess anticancer properties. However, the efficacy of PPARc ligands varies in different cancers. In colon cancer, the role of PPARc and its ligands is controversial. We recently showed that downregulation of X-linked inhibitor of apoptosis protein (XIAP) could sensitize colon cancer cells to troglitazone, and 15-deoxy-D12,14-prostaglandin J2 (15-PGJ2) induced cell killing. In our study, we aimed to examine whether rosiglitazone, another more clinically relevant PPARc ligand, has any synergistic anticancer effect with XIAP downregulation in colon cancer. Human colon cancer cell lines HCT116-XIAP 1/1 cells and HCT116-XIAP 2/2 cells were treated with various concentrations of rosiglitazone. The effects of rosiglitazone on cell proliferation, apoptosis and growth of xenograft colon cancers were studied. Rosiglitazone barely suppressed the growth and only very weakly induced apoptosis in HCT116 cells in vitro. Loss of XIAP did not sensitize HCT116 cells to rosiglitazone-induced growth inhibition or apoptosis. In vivo studies revealed that rosiglitazone strongly suppressed the growth of xenograft colon cancer, especially tumors derived from HCT116-XIAP 2/2 cells. The rosiglitazone-treated tumor had reduced expression of ki-67 and lowered mitotic rate. Downregulation of XIAP was associated with an impaired activation of PPARc by its ligand. Rosiglitazone induced marked upregulation of PTEN in HCT116-XIAP 2/2 cells, as well as in xenograft tumors derived from HCT116-XIAP 2/2 cells. We concluded that rosiglitazone significantly suppresses the growth of xenograft colon cancer, and downregulation of XIAP sensitizes the xenograft tumors to rosiglitazone-induced tumor suppression in vivo via upregulation of PTEN.

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Ligands for the peroxisome proliferator-activated receptor-γ have inhibitory effects on growth of human neuroblastoma cells in vitro

Cited by 32 publications

References 40 publications

Rosiglitazone enhances fluorouracil-induced apoptosis of HT-29 cells by activating peroxisome proliferator-activated receptor γ

Rosiglitazone enhances fluorouracil-induced apoptosis of HT-29 cells by activating peroxisome proliferator-activated receptor γ

Antineoplastic effects of rosiglitazone and PPARγ transactivation in neuroblastoma cells

Loss of XIAP sensitizes rosiglitazone‐induced growth inhibition of colon cancer in vivo

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