Antiproliferative effects of the histone deacetylase inhibitor FR901228 on small‐cell lung cancer lines and drug‐resistant sublines

Tsurutani, Junji; Soda, Hiroshi; Oka, M.; Suenaga, Mitsuhiro; Doi, Seiji; Nakamura, Yoichi; Nakatomi, Katsumi; Shiozawa, Ken; amada, Yasuaki Y; Kamihira, Shimeru; Kohno, Shigeru

doi:10.1002/ijc.10921

Cited by 38 publications

(35 citation statements)

References 23 publications

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“…These data, together with previous studies in other cellular (28,38,39) and animal cancer models (36,37,51), suggest that the histone deacetylase inhibitors could be useful as antineoplastic agents for the treatment of human pancreatic adenocarcinoma.…”

Section: Discussionsupporting

confidence: 61%

“…Results from our group and others (28,38,39) have shown that histone deacetylase inhibitors were able to induce apoptosis in drug-resistant tumor cells from different tissues. The results presented herein show that histone deacetylase inhibitors were able to induce massive apoptosis in the three pancreatic adenocarcinoma cell lines, independently of their intrinsic resistance to other anticancer drugs.…”

Section: Discussionmentioning

confidence: 82%

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Histone deacetylase inhibitors induced caspase-independent apoptosis in human pancreatic adenocarcinoma cell lines

García-Morales

Gómez-Martínez

Carrato

et al. 2005

Molecular Cancer Therapeutics

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The antitumor activity of the histone deacetylase inhibitors was tested in three well-characterized pancreatic adenocarcinoma cell lines, IMIM-PC-1, IMIM-PC-2, and RWP-1. These cell lines have been previously characterized in terms of their origin, the status of relevant molecular markers for this kind of tumor, resistance to other antineoplastic drugs, and expression of differentiation markers. In this study, we report that histone deacetylase inhibitors induce apoptosis in pancreatic cancer cell lines, independently of their intrinsic resistance to conventional antineoplastic agents. The histone deacetylase inhibitorinduced apoptosis is due to a serine protease -dependent and caspase-independent mechanism. Initially, histone deacetylase inhibitors increase Bax protein levels without affecting Bcl-2 levels. Consequently, the apoptosisinducing factor (AIF) and Omi/HtrA2 are released from the mitochondria, with the subsequent induction of the apoptotic program. These phenomena require AIF relocalization into the nuclei to induce DNA fragmentation and a serine protease activity of Omi/HtrA2. These data, together with previous results from other cellular models bearing the multidrug resistance phenotype, suggest a possible role of the histone deacetylase inhibitors as antineoplastic agents for the treatment of human pancreatic adenocarcinoma. [Mol Cancer Ther 2005; 4(8);1222 -30]

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Section: Discussionsupporting

confidence: 61%

Section: Discussionmentioning

confidence: 82%

Histone deacetylase inhibitors induced caspase-independent apoptosis in human pancreatic adenocarcinoma cell lines

García-Morales

Gómez-Martínez

Carrato

et al. 2005

Molecular Cancer Therapeutics

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“…Reversible histone deacetylase inhibitors, such as trichostatin A, were shown to modulate the IGF axis (54,55), potentially by induction of IGFbinding protein-3, which is the major binding protein for IGF-II and also induces apoptosis in a p53-independent manner (56). Trichostatin A analogs have already entered clinical trials for several carcinomas including breast, colon, prostate, and lung cancer (57,58). Because dysregulation of the IGF-II transcription has been connected in some HCCs with genomic imprinting (40), remethylation strategies (e.g., by budesonide) also may decrease expression of IGF-II (59).…”

Section: Discussionmentioning

confidence: 99%

Molecular Profiling of Human Hepatocellular Carcinoma Defines Mutually Exclusive Interferon Regulation and Insulin-Like Growth Factor II Overexpression

et al. 2004

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“…91 In contrast, other studies reported that HDACIs suppressed rather than activated hTERT expression in prostate cancer cells treated with TSA. 92 Therefore, the net effect of HDACIs may depend on the cell type and the particular inhibitor used. The other concern is that HDACIs may enhance chromosomal instability.…”

Section: Anti-tumor Activity Of Hdacismentioning

confidence: 99%

Histone Deacetylase Inhibitors for Cancer Therapy

Kim¹,

Bang²,

Robertson³

2006

Epigenetics

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The epigenome of cancer cells is determined by DNA methylation and an array of post-translational modifications of the core histones. Epigenetic abnormalities are commonly found in human tumors and importantly, they can be reversed by pharmacologic inhibitors. Histone deacetylase inhibitors (HDACIs) represent one of the most promising epigenetic treatments for cancer. HDACIs have emerged as promising targets for cancer therapy because they reactivate the transcription of multiple genes that are silenced in human tumors and they show pleiotropic anti-tumor effects selectively in cancer cells. HDACIs are well-tolerated and several show promising anti-tumor activity. While gene transcription has been considered to be the major target of HDACIs, inhibition of acetylation of non-histone proteins is now emerging as a novel basis for their anti-tumor effects. In this review, we discuss new insights into the molecular mechanism of HDACIs, their current status of clinical development, and possible future uses in cancer therapy.

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Antiproliferative effects of the histone deacetylase inhibitor FR901228 on small‐cell lung cancer lines and drug‐resistant sublines

Abstract: FR901228 is a novel histone deacetylase (HDAC) inhibitor

Cited by 38 publications

References 23 publications

Histone deacetylase inhibitors induced caspase-independent apoptosis in human pancreatic adenocarcinoma cell lines

Histone deacetylase inhibitors induced caspase-independent apoptosis in human pancreatic adenocarcinoma cell lines

Molecular Profiling of Human Hepatocellular Carcinoma Defines Mutually Exclusive Interferon Regulation and Insulin-Like Growth Factor II Overexpression

Histone Deacetylase Inhibitors for Cancer Therapy

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