Sodium Butyrate Increases Expression of the Coxsackie and Adenovirus Receptor in Colon Cancer Cells

Küster, Katrin; Grötzinger, Carsten; Koschel, Annika; Fischer, Andréas; Wiedenmann, Bertram; Anders, Mario

doi:10.3109/07357900902783195

Cited by 10 publications

(8 citation statements)

References 31 publications

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“…ASCL1 and CgA) and induces cell cycle arrest significantly, alters tumor cell proliferation and apoptosis in pheochromocytoma, which were indicated by the levels of cyclin D1, p21, cleaved PARP and cleaved caspase-3 proteins (30). NaBu also increases expression of the coxsackie and adenovirus receptor in colon cancer cells (31). Although some researchers have reported that NaBu induces human colon carcinoma HT-29 cell apoptosis through a mitochondrial pathway (32), we found a new relational molecular, ASC, whose expression was recovered in LS174T cells.…”

Section: Discussionmentioning

confidence: 53%

Sodium butyrate restores ASC expression and induces apoptosis in LS174T cells

Zhang

Bai

Ren

et al. 2012

International Journal of Molecular Medicine

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Abstract. Sodium butyrate (NaBu) is a short-chain fatty acid (SCFA), which has been proposed as a potential anticancer agent. Apoptosis-associated speck-like protein (ASC) is a pro-apoptotic signaling factor that is subjected to epigenetic silencing in human cancers. Modulation by the aberrant methylation of CpG islands of ASC is a well-characterized epigenetic mechanism, and the methylation-induced silencing of ASC has been observed in several types of tumors. NaBu induces cell cycle arrest, markers of cell differentiation and apoptosis in colon cancer. NaBu promotes transcriptional activation by relaxing the DNA conformation and displays anti-proliferative and differentiating activity in a wide variety of cancers. Thus, we used NaBu to investigate the relationship between the status of cell proliferation and the re-expression of ASC in colon carcinoma LS174T cells. Our experiments determined ASC re-expression at the protein level using western blotting. In addition, we used reverse transcriptionpolymerase chain reaction to detect the expression levels of ASC mRNA and an MTT assay to detect the inhibitory rate of cell growth. The apoptosis rate was also detected for further validation of the re-expression of ASC. The results showed that ASC re-expression was significantly increased in the LS174 cells following NaBu treatment in a time-and dose-dependent manner. The expression of ASC also induced the apoptosis of LS174T cells. These results suggest that NaBu plays a role in the reactivation of ASC expression and that the latter promotes the apoptosis of LS174T cells.

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Section: Discussionmentioning

confidence: 53%

Sodium butyrate restores ASC expression and induces apoptosis in LS174T cells

Zhang

Bai

Ren

et al. 2012

International Journal of Molecular Medicine

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“…To date, mainly CAR downregulation in cancer types has been investigated. Hereby, activation of the Raf/MEK/ERK pathway and TGF- β signalling, hypoxia, epithelial–mesenchymal transdifferentiation and histone deacetylation of the CAR gene promoter were identified as regulators of CAR expression (Brüning and Runnebaum, 2003; Pong et al , 2003; Anders et al , 2003a; Lacher et al , 2006; Küster et al , 2010a, 2010b; Lacher et al , 2011). In contrast, few studies have investigated the mechanism of CAR upregulation.…”

Section: Discussionmentioning

confidence: 99%

“…In line with these observations, significant correlations between impaired CAR expression and a poor clinical outcome for gastric and bladder cancer patients were found (Matsumoto et al , 2005; Anders et al , 2009). Regulation of declined CAR expression in cancers has been attributed to activation of the Raf/MEK/ERK pathway and the TGF- β signalling, as well as hypoxia, epithelial–mesenchymal transdifferentiation and histone deacetylation of the CAR gene promoter (Brüning and Runnebaum, 2003; Pong et al , 2003; Anders et al , 2003a; Lacher et al , 2006; Küster et al , 2010a, 2010b; Lacher et al , 2011). …”

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confidence: 99%

Presence of the Coxsackievirus and Adenovirus Receptor (CAR) in human neoplasms: a multitumour array analysis

et al. 2013

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Background:The Coxsackie- and Adenovirus Receptor (CAR) has been assigned two crucial attributes in carcinomas: (a) involvement in the regulation of growth and dissemination and (b) binding for potentially therapeutic adenoviruses. However, data on CAR expression in cancer types are conflicting and several entities have not been analysed to date.Methods:The expression of CAR was assessed by immunohistochemical staining of tissue microarrays (TMA) containing 3714 specimens derived from 100 malignancies and from 273 normal control tissues.Results:The expression of CAR was detected in all normal organs, except in the brain. Expression levels, however, displayed a broad range from being barely detectable (for example, in the thymus) to high abundance expression (for example, in the liver and gastric mucosa). In malignancies, a high degree of variability was notable also, ranging from significantly elevated CAR expression (for example, in early stages of malignant transformation and several tumours of the female reproductive system) to decreased CAR expression (for example, in colon and prostate cancer types).Conclusion:Our results provide a comprehensive insight into CAR expression in neoplasms and indicate that CAR may offer a valuable target for adenovirus-based therapy in a subset of carcinomas. Furthermore, these data suggest that CAR may contribute to carcinogenesis in an entity-dependent manner.

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“…Histone deacetylation inhibitors are anti-neoplastic agents acting by net acetylation of core histones, causing the uncoiling of chromatin and activation of numerous genes implicated in the regulation of cell survival, growth, differentiation, cell cycle arrest and apoptosis (7,8,12,13). The activity of G 1 Cdks is stringently regulated by NaB through association with specific Cdk inhibitors including the CIP/KIP family (p21 ), which could bind all G 1 cyclin-Cdk complexes (8,14).…”

Section: Discussionmentioning

confidence: 99%

Trastuzumab enhances the anti-tumor effects of the histone deacetylase inhibitor sodium butyrate on a HER2-overexpressing breast cancer cell line

Chen

Feng²,

Xu³

et al. 2011

Int J Mol Med

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Abstract. Trastuzumab has efficacy to improve the effect of cytotoxic drugs, such as paclitaxel and anthracyclin, against HER2-overexpressing breast cancer cells. Sodium butyrate (NaB), a histone deacetylase inhibitor, is known to have antitumoral properties. However, whether and how trastuzumab possesses the potential to synergize the anti-tumor effect of NaB on breast cancer cells is still equivocal. To elucidate whether combined treatment with NaB and trastuzumab exerts antitumor effects on a HER2-overexpressing breast cancer cell line, SKBR3 cells were treated with NaB alone or in combination with trastuzumab, and the effects on proliferation and cell cycle progression were analyzed. Combinatory treatment with NaB (4 mmol/l) and trastuzumab (20 µg/ml) significantly increased the growth-inhibitory effect on SKBR3 breast cancer cells, in comparison to NaB or trastuzumab treatment alone. The growthinhibitory effect of the combination of NaB and trastuzumab was accompanied by elevated mRNA and protein levels of the cyclin-dependent kinase inhibitor p27 Kip1 . In contrast, this effect was absent in HER2-negative HCC1937 cells. In conclusion, trastuzumab significantly improved the antitumor effect of NaB on HER2-overexpressing breast cancer cell line in vitro.

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Sodium Butyrate Increases Expression of the Coxsackie and Adenovirus Receptor in Colon Cancer Cells

Cited by 10 publications

References 31 publications

Sodium butyrate restores ASC expression and induces apoptosis in LS174T cells

Sodium butyrate restores ASC expression and induces apoptosis in LS174T cells

Presence of the Coxsackievirus and Adenovirus Receptor (CAR) in human neoplasms: a multitumour array analysis

Trastuzumab enhances the anti-tumor effects of the histone deacetylase inhibitor sodium butyrate on a HER2-overexpressing breast cancer cell line

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