PPAR-γ agonist increase gefitinib's antitumor activity through PTEN expression

Lee, Sung Yong; Hur, Gyu Young; Jung, Ki Hwan; Jung, Haeil; Lee, Sang Yeub; Kim, Je Hyeong; Shin, Chol; Shim, Jae Jeong; In, Kwang Ho; Kang, Kyung Ho; Yoo, Se Hwa

doi:10.1016/j.lungcan.2005.10.010

Cited by 87 publications

(73 citation statements)

References 12 publications

(12 reference statements)

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“…The activation of Akt only after prolonged berberine treatment indicated a relatively slow effect on PTEN expression, likely through transcription regulation ( Figure 5D and Supplementary information, Figure S2). It is reported that berberine inhibits PPARγ activity by increasing PPARγ phosphorylation [7,8] and PTEN transcrip- tion is regulated by PPARγ [31,32]. The inhibition of PPARγ by berberine was clearly illustrated by berberinemediated inhibition of 3T3-L1 adipocyte differentiation, as PPARγ is one of the most important transcription factors in adipocyte differentiation ( Figure 6A) [7,8,33,34].…”

Section: Berberine Induces Sr-a Expression By Activating Pi3-kinase Smentioning

confidence: 85%

Berberine promotes the development of atherosclerosis and foam cell formation by inducing scavenger receptor A expression in macrophage

Yao

Zheng

et al. 2009

Cell Res

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Section: Berberine Induces Sr-a Expression By Activating Pi3-kinase Smentioning

confidence: 85%

Berberine promotes the development of atherosclerosis and foam cell formation by inducing scavenger receptor A expression in macrophage

Yao

Zheng

et al. 2009

Cell Res

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“…Recent evidence has demonstrated that PPARγ activation by TZDs inhibits cell growth and induces cell apoptosis in liver cancer cell lines [24,25] . Moreover, rosiglitazone, as a PPARγ synthetic ligand, has been shown to enhance the antitumor www.chinaphar.com Cao LQ et al Acta Pharmacologica Sinica npg activity of some chemotherapeautic drugs by the modulation of cancer cell agents [26,27] . However, the effects of rosiglitazone on hepatoma cells have been poorly understood until now.…”

Section: Discussionmentioning

confidence: 99%

Rosiglitazone sensitizes hepatocellular carcinoma cell lines to 5-fluorouracil antitumor activity through activation of the PPARγ signaling pathway

Cao

Wang²,

Wang

et al. 2009

Acta Pharmacol Sin

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Aim: Resistance to 5-fluorouracil (5-FU) is a major cause of chemotherapy failure in advanced hepatocellular carcinoma (HCC). Rosiglitazone, a peroxisome proliferator-activated receptor γ (PPARγ) agonist, has a crucial role in growth inhibition and induction of apoptosis in several carcinoma cell lines. In this study, we examine rosiglitazone-induced sensitization of HCC cell lines (BEL-7402 and Huh-7 cells) to 5-FU. Methods: The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay was used to evaluate cell viability. Western blotting analysis was performed to detect the protein expression (PPARγ, PTEN, and COX-2) in BEL-7402 cells. Immunohistochemistry staining was used to examine the expression of PTEN in 100 advanced HCC tissues and paracancerous tissues. In addition, small interfering RNA was used to suppress PPARγ, PTEN, and COX-2 expression. Results: Rosiglitazone facilitates the anti-tumor effect of 5-FU in HCC cell lines, which is mediated by the PPARγ signaling pathway. Activation of PPARγ by rosiglitazone increases PTEN expression and decreases COX-2 expression. Since distribution of PTEN in HCC tissues is significantly decreased compared with the paracancerous tissue, over-expression of PTEN by rosiglitazone enhances 5-FU-inhibited cell growth of HCC. Moreover, down-regulation of COX-2 is implicated in the synergistic effect of 5-FU. Conclusion: Rosiglitazone sensitizes hepatocellular carcinoma cell lines to 5-FU antitumor activity through the activation of PPARγ. The results suggest potential novel therapies for the treatment of advanced liver cancer.

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“…51 PPARγ ligands have also been shown to inhibit lung carcinoma cell proliferation through increased expression of PTEN and p21. 52,53 In other studies, rosiglitazone reduced phosphorylation of Akt and increased PTEN protein expression in non small-cell lung cancer (NSCLC) cells, and this was associated with inhibition of tumor cell proliferation through PPARγ-dependent signals. 54 PPARγ agonists have also been shown to target cyclin-dependent kinase (CDK) inhibitors such as p18, p21 and p27 during adipogenesis in normal cells and hepatocellular carcinoma cell lines.…”

Section: Role In Cancer Biologymentioning

confidence: 95%

Peroxisome proliferator-activated receptor γ in bladder cancer: A promising therapeutic target

Mansure¹,

Nassim²,

Kassouf³

2009

Cancer Biology & Therapy

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PPAR-γ agonist increase gefitinib's antitumor activity through PTEN expression

Cited by 87 publications

References 12 publications

Berberine promotes the development of atherosclerosis and foam cell formation by inducing scavenger receptor A expression in macrophage

Berberine promotes the development of atherosclerosis and foam cell formation by inducing scavenger receptor A expression in macrophage

Rosiglitazone sensitizes hepatocellular carcinoma cell lines to 5-fluorouracil antitumor activity through activation of the PPARγ signaling pathway

Peroxisome proliferator-activated receptor γ in bladder cancer: A promising therapeutic target

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