The combination effect of sodium butyrate and 5-Aza-2'-deoxycytidine on radiosensitivity in RKO colorectal cancer and MCF-7 breast cancer cell lines

Cho, Hang Joo; Kim, Sin Young; Kim, Kee Hwan; Kang, Won Kyung; Kim, Ji Il; Oh, Seong Tack; Kim, Jeong Soo; An, Chang Hyeok

doi:10.1186/1477-7819-7-49

Cited by 33 publications

(28 citation statements)

References 28 publications

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“…Gene silencing associated with the aberrant methylation of promoter region of CpG islands is an acquired epigenetic alteration that serves as an alternative to genetic events in the inactivation of tumor suppressor and other genes in human cancers. NaBu has been applied in cellular and molecular research (23,24), particularly in antitumor research (25)(26)(27)(28). It plays a vital role in vitamin D-induced apoptosis through PTEN upregulation, which has potential benefit in gastric cancer therapy (29).…”

Section: Discussionmentioning

confidence: 99%

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: 99%

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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“…[8][9][10][11] In addition, there are some reports that the combined therapy of DNA methylation inhibitor or histone deacetylase (HDAC) inhibitor and anticancer drugs resulted in synergistic growth inhibitory effects on cancer cells. [12][13][14] Reportedly, some solute carrier (SLC) transporters are also involved in the transport of anticancer drugs. 15,16) However, there is little information on the transcriptional regulation of SLC transporter gene expression through epigenetic mechanisms in colon cancer cells.…”

mentioning

confidence: 99%

Different Involvement of DNA Methylation and Histone Deacetylation in the Expression of Solute-Carrier Transporters in 4 Colon Cancer Cell Lines

Ikehata

Iwakawa

2012

Biological & Pharmaceutical Bulletin

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The purpose of this study on the involvement of epigenetic control of the expression of solute carrier (SLC) transporters by DNA methylation and histone deacetylation in 4 colon cancer cells is to find the epigenetic control mechanisms of drug transporters in colon cancers. Human colon cancer cell lines (HCT116, HT29, SW48, SW480) were treated with 5-aza-2′-deoxycytidine (DAC), as a DNA methyltransferase inhibitor, followed by trichostatin A (TSA), as a histone deacetylase inhibitor. The mRNA expression and DNA methylation of several SLC transporters were analyzed by real-time polymerase chain reaction (PCR) and methylation-specific PCR, respectively. Among 12 SLC transporters possessing cytosine-phosphate-guanine (CpG) islands, thiamine transporter 2 (THTR2) (SLC19A3) gene showed a correlation between its mRNA expression level and DNA methylation status. TSA treatment increased histone H3 acetylation of THTR2 promoter region in all 4 colon cancer cell lines examined. HCT116 and SW48 cells showed a lack of THTR2 mRNA expression and methylation of its promoter, and DAC treatment induced its re-expression. In addition, the co-treatment with DAC and TSA increased THTR2 mRNA expression more markedly than DAC treatment in HCT116 and SW48 cells. In HT29 and SW480 cells that showed little methylation of THTR2 promoter, TSA treatment induced THTR2 mRNA expression markedly, but DAC treatment did not. In the 4 colon cancer cells examined, THTR2 mRNA expression is down-regulated by DNA methylation and/or histone deacetylation.Key words solute-carrier transporter; DNA methylation; histone deacetylation; colon cancer; epigenetics; cytosine-phosphate-guanine island Epigenetics refers to heritable changes in gene expression that are not coded in the DNA sequence itself. Epigenetic events include methylation of DNA and modifications to histone proteins. The disruption of epigenetic mechanisms such as DNA methylation and histone acetylation can lead to inappropriate expression or silencing of genes, resulting in several major diseases including cancer. In tumors in particular, DNA hypermethylation in cytosine-phosphate-guanine (CpG) islands in the promoter region of a specific gene is often observed. This phenomenon leads to transcriptional downregulation of cancer-related genes like tumor suppressor genes.

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“…Bütirat H3 ve H4'ün hiperasetilasyonuna yol açar. Sodyum bütirat, MCF-7 meme kanseri hücre serisi hatlarının radiosensitivitesini artırabilir ve kaspaz-10 ekspresyonu ile apoptozu tetikleyebilir 67,68 . Bunun yanı sıra bütirat spinal müsküler atrofide 69,70,71 , myelodisplastik sendromda 72 ve metabolik hastalıkların tanısal yaklaşımında kullanabilirliği ile ilgili çalışmalar yapılmıştır 73 .…”

Section: Kısa Zincirli Yağ Asitleriunclassified

Meme Kanserinde Epigenetik Tedavi

Eroğlu

2018

Arşiv Kaynak Tarama Dergisi

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Cancer progression can be controlled by both genetic and epigenetic alterations. Only epigenetic alterations are reversible unlike the genetic alterations. This can be a important advantage to suggest that epigenetic modifications should be preferred in therapy applications. DNA methyltransferases and histone deacetylases have become the primary targets for studies in epigenetic therapy. The US Food and Drug Administration approved some DNA methylation inhibitors and histone deacetylation inhibitors as anti-cancer drugs. Therefore, the uses of epigenetic targets are believed to have great potential as a lasting favorable approach in treating breast cancer.

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The combination effect of sodium butyrate and 5-Aza-2'-deoxycytidine on radiosensitivity in RKO colorectal cancer and MCF-7 breast cancer cell lines

Cited by 33 publications

References 28 publications

Sodium butyrate restores ASC expression and induces apoptosis in LS174T cells

Sodium butyrate restores ASC expression and induces apoptosis in LS174T cells

Different Involvement of DNA Methylation and Histone Deacetylation in the Expression of Solute-Carrier Transporters in 4 Colon Cancer Cell Lines

Meme Kanserinde Epigenetik Tedavi

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