Activation of peroxisome proliferator‐activated receptor‐γ by troglitazone (TGZ) inhibits human lung cell growth

Li, Mingyue; Lee, Tak W.; Mok, Tony; Warner, Timothy D.; Yim, Anthony P.C.; Chen, George G.

doi:10.1002/jcb.20474

Cited by 61 publications

(64 citation statements)

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“…The human nonsmall cell lung cancer (NSCLC) cells, NCI-H23, were grown in 100-mm tissue culture disks as previously described [19].…”

Section: Cell Culturementioning

confidence: 99%

“…Cell proliferation was measured with dimethylthiazolyldiphenyltetrazolium-bromide (MTT) as previously described [19]. Cell proliferation was further confirmed by bromodeoxyuridine labelling of DNA, performed according to the manufacturer's instructions (Roche Applied Science, Penzberg, Germany).…”

Section: Assessment Of Cell Proliferation and Deathmentioning

confidence: 99%

“…The mitogen-activated protein kinase (MAPK) family of proteins, including c-Jun NH 2 -terminal kinase (JNK), extracellular signal-regulated kinase (ERK) and p38 MAPK, play an important role in cell survival and apoptosis. The activation of the MAPK pathway can be either anti-apoptotic or proapoptotic, depending on the cellular context [17][18][19]. Considering the tumour-promoting effect of NNK in the lung, the aim of the present study was to investigate the roles of NFkB and MAPK in NNK-mediated lung carcinogenesis.…”

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confidence: 99%

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Haem oxygenase-1 plays a central role in NNK-mediated lung carcinogenesis

Li¹,

Yip²,

Hsin³

et al. 2008

Eur Respir J

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The tobacco-specific nitrosamine, 4-(N-methyl-N-nitrosoamino)-1-(3-pyridyl)-1-butanone (NNK), is a potent lung cancer inducer. However, how NNK induces lung cancer is still largely unknown.Haem oxygenase (HO)-1 was evaluated in 30 pairs of lung cancer tumour samples and matched nontumour tissues from patients with a history of cigarette smoking. Expression of p21 Cip1/Waf1/Cid1 (p21), B-cell lymphoma (Bcl)-2 family members, mitogen-activated protein kinase and nuclear factor (NF)-kB was also studied in lung cancer cells treated with NNK.The levels of HO-1 and p21 were significantly increased in lung tumour tissues. There was a positive relationship between these two proteins in the tumour. NNK stimulated lung cell proliferation and elevated the levels of HO-1, p21, inhibitor of apoptosis protein (c-IAP)2 and Bcl-2, but downregulated Bad. These effects of NNK were blocked by zinc protoporphyrin-XII, an HO-1 inhibitor. The NNK-mediated expression of HO-1 was governed by NF-kB and extracellular signal-regulated kinase 1/2, since blocking either of these prevented the stimulatory effect of NNK on HO-1, as well as molecules downstream of HO-1, such as p21, c-IAP2, Bcl-2 and Bad.In conclusion, haem oxygenase-1 plays a central role in NNK-mediated cell proliferation by promoting the expression of p21Cip1/Waf1/Cid1 , inhibitor of apoptosis protein 2 and B-cell lymphoma-2 but inhibiting the activity of Bad. Nuclear factor-kB and extracellular signal-regulated kinase 1/2 function upstream of haem oxygenase-1. Therefore, haem oxygenase-1 is likely to be a potential target in the treatment of smoking-related lung cancer.

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“…The human nonsmall cell lung cancer (NSCLC) cells, NCI-H23, were grown in 100-mm tissue culture disks as previously described [19].…”

Section: Cell Culturementioning

confidence: 99%

Section: Assessment Of Cell Proliferation and Deathmentioning

confidence: 99%

mentioning

confidence: 99%

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Haem oxygenase-1 plays a central role in NNK-mediated lung carcinogenesis

Li¹,

Yip²,

Hsin³

et al. 2008

Eur Respir J

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“…Recently, it has been found that PPARÁ is overexpressed in various types of tumor cells and PPARÁ agonists can induce apoptosis (44,45). It has been reported that ChR derivatives induce apoptosis of human hepatocellular carcinoma and human gastric cancer cells by activating PPARÁ (17,18).…”

Section: Discussionmentioning

confidence: 99%

Induction of apoptosis by 5,7-dihydroxy-8-nitrochrysin in breast cancer cells: The role of reactive oxygen species and Akt

Zhao

Tian²,

Cao³

et al. 2010

Int J Oncol

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Abstract. 5,7-dihydroxy-8-nitrochrysin (NOC), a novel synthetic chrysin analogue, induces apoptosis in human cancer cells. We previously demonstrated that NOC possesses stronger cytotoxicity towards human colon carcinoma and human gastric carcinoma cells than chrysin. Herein, we demonstrate the mechanism by which NOC preferentially suppresses the viability of the MDA-MB-453 human breast cancer cell line (ER negative, Her2 overexpressing) and moderately suppresses the viability of the MCF-7 cell line (ER positive, Her2 low), but has little effect on the immortalized non-cancerous HBL-100 breast cell line (ER positive, Her2 low). Moreover, the results of our studies, for the first time, provide mechanistic evidence that NOC induces apoptosis by the generation of reactive oxygen species and Akt dephosphorylation. Our findings highlight a new mechanism responsible for NOC-induced apoptosis, and raise the possibility that NOC might be promising as a candidate for human breast cancer therapy.

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“…Further, ciglitazone is reported to induce differentiation and apoptosis in non small cell lung cancer [16]. In addition, the TZDs have been found to decrease lung cancer induced angiogenesis and to limit proliferation [17]. We recently have found that different TZDs have the capacity to modulate arachidonic acid metabolism by a variety of pathways [18].…”

Section: Introductionmentioning

confidence: 99%