The Histone Deacetylase Inhibitor Suberoylanilide Hydroxamic Acid Induces Apoptosis via Induction of 15-Lipoxygenase-1 in Colorectal Cancer Cells

Hsi, Linda C.; Xi, Xiaopei; Lotan, Reuben; Shureiqi, Imad; Lippman, Scott M.

doi:10.1158/0008-5472.can-04-1867

Cited by 59 publications

(58 citation statements)

References 15 publications

(21 reference statements)

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“…Similarly, the percentages of early apoptotic cells treated with sodium butyrate were reduced following exposure to 15-Lox-1 inhibitor. The similar results were reported previously on the involvement of 15-Lox-1 in the HDAC inhibitor-induced apoptosis in colorectal cancer (Hsi et al 2004). Moreover, treatment of cells with sodium butyrate resulted in a significant increase in the gene expression of 15-Lox-1 in both cell lines.…”

Section: Discussionsupporting

confidence: 90%

“…Data represent the mean ± SD of three separate experiments. Statistical differences between treated and untreated cells were analyzed by ANOVA (*P \ 0.05; **P \ 0.01; ***P \ 0.001) 15-Lox-1 was accompanied by elevation of 13(S)-HODE, inhibition of growth and induction of apoptosis in the mentioned cells (Hsi et al 2004). Acetylation is a well-studied molecular mechanism mediating epigenetic modulation of genes depending on the balance between activity of histone deacetylase and histone acetyl transferase (Haberland et al 2009).…”

Section: Discussionmentioning

confidence: 99%

“…The data represent mean ± SD of three separate experiments. Statistical differences between sodium butyrate-treated and untreated groups were analyzed by ANOVA (*P \ 0.05; **P \ 0.01) inhibitors on the regulation of 15-Lox-1 pathway has been exhibited in colorectal cancer (Hsi et al 2004). Breast cancer is considered as a remarkable cause of cancer-related mortality among women in the world and many efforts are focused on improving therapeutic strategies.…”

Section: Discussionmentioning

confidence: 99%

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Involvement of 15-lipoxygenase-1 in the regulation of breast cancer cell death induced by sodium butyrate

et al. 2016

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15-Lipoxygenase-1 (15-Lox-1) as a member of fatty acid dioxygenases family has received considerable attention as an effector of cancer cell growth. The relevance of sodium butyrate on 15-Lox-1 pathway has not been determined in breast cancer. This study is aimed to investigate the possible involvement of 15-Lox-1 in the regulation of breast cancer cell growth by sodium butyrate. MTT assay was used to assess the cytotoxicity effect and Annexin-V-FITC staining was applied for detection of apoptosis using flow cytometry. The involvement of 15-Lox-1 was examined using 15-Lox-1 specific inhibitor and enzyme gene expression level and activity was further analyzed by Real-time PCR and measurement of 13(S)-HODE. The results revealed that sodium butyrate increased the expression of 15-Lox-1 and production of 13(S)HODE. 15-Lox-1 was also involved in the sodium butyrate-induced breast cancer cell cytotoxicity and apoptosis. This study provided more evidences on the positive effectiveness of 15-Lox-1/13(S)-HODE on controlling growth of breast cancer cells.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Involvement of 15-lipoxygenase-1 in the regulation of breast cancer cell death induced by sodium butyrate

et al. 2016

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“…Restoring 15-LOX-1 and 13-S-HODE expressions by various means has been shown to restore and be mechanistically linked to apoptosis in colorectal cancer cells (18,20,21). We showed recently that low micromolar concentrations of the histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid induces 15-LOX-1 expression as a mechanism of apoptosis induction in human colon cancer cells (21), providing the first demonstration of a mechanistic link between HDAC-induced 15-LOX-1 and apoptosis in carcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

The methyltransferase inhibitor 5-aza-2-deoxycytidine induces apoptosis via induction of 15-lipoxygenase-1 in colorectal cancer cells

Hsi

et al. 2005

Molecular Cancer Therapeutics

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DNA methylation by DNA methyltransferases in CpGrich promoter regions of genes is a well-described component of epigenetic silencing in human cells. Dysregulation of this process in cancer cells may lead to hypermethylation of promoter CpG islands, thus disabling transcription initiation of certain genes, such as tumor suppressor genes. Reversing epigenetic silencing and up-regulating genes involved in preventing or reversing the malignant phenotype has become a new, important targeted approach for cancer prevention and treatment. Therefore, methyltransferase inhibitors (MTI) have emerged recently as promising chemotherapeutic or preventive agents. The potent MTI 5-aza-2-deoxycytidine (5-Azadc) causes growth arrest, differentiation, and/or apoptosis of many tumor types in vitro and in vivo. The present study shows that low micromolar concentrations of 5-Azadc induce the expression of 15-lipoxygenase-1 (15-LOX-1) in human colorectal cancer cells. The expression of 15-LOX-1 correlates with 5-Azadc-induced increases in 13-S-hydroxyoctadecadienoic acid levels, growth inhibition, and apoptosis in these cells. Furthermore, specific inhibition of 15-LOX-1 by pharmacologic means or small interfering RNA significantly reduced the 5-Azadc-induced effects. These novel findings are the first demonstration of a mechanistic link between the induction of 15-LOX-1 by a MTI and apoptosis in cancer cells. This result has important implications for the study of 5-Azadc and other MTIs in the prevention and therapy of colorectal cancer and supports future investigations of the mechanisms by which MTIs up-regulate 15-LOX-1. [Mol Cancer Ther 2005;4(11):1740 -6]

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“…Shirakawa et al reviews at least 18 different HDAC inhibitors. 46,47 SAHA has been shown to produce positive results when used to treat HDAC involved in prostate cancer, 34 breast cancer, 35,36 pancreatic cancer, 37 various leukemias, 38 colorectal cancer, 39 mesothelioma, 40 head and neck cancers, 41 as well as HIV infections 42 and in models of Huntington's disease. 43 Further studies are needed to determine if SAHA is effective against other specific HDACs and to determine the potential side effects of treatment.…”

Section: Resultsmentioning

confidence: 99%

Epstein-Barr Virus (EBV) and the Effectiveness of Suberoylanilide Hydroxamic Acid (SAHA) as a Treatment for EBV Infection and Associated Cancers

Bart¹,

Johnson²,

DeGol³

et al. 2013

Advances in Tumor Virology

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Since being discovered in 1964, Epstein-Barr virus (EBV) has become a growing concern. Clinically, EBV is responsible for many diseases, most notably infectious mononucleosis. In addition to mononucleosis, EBV causes several cancers such as Hodgkin's lymphoma, Burkitt's lymphoma, and nasopharyngeal carcinoma (NPC). Suberoylanilide hydroxamic acid (SAHA) is an anti-cancer drug that inhibits growth and proliferation of various EBV-related cancers. SAHA acts as a histone deacetylase (HDAC) inhibitor. The responsiveness of SAHA treatment stems from the induction of EBV's lytic cycle.

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The Histone Deacetylase Inhibitor Suberoylanilide Hydroxamic Acid Induces Apoptosis via Induction of 15-Lipoxygenase-1 in Colorectal Cancer Cells

Abstract: ABSTRACT

Cited by 59 publications

References 15 publications

Involvement of 15-lipoxygenase-1 in the regulation of breast cancer cell death induced by sodium butyrate

Involvement of 15-lipoxygenase-1 in the regulation of breast cancer cell death induced by sodium butyrate

The methyltransferase inhibitor 5-aza-2-deoxycytidine induces apoptosis via induction of 15-lipoxygenase-1 in colorectal cancer cells

Epstein-Barr Virus (EBV) and the Effectiveness of Suberoylanilide Hydroxamic Acid (SAHA) as a Treatment for EBV Infection and Associated Cancers

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