Epigenetic Modifications: Therapeutic Potential in Cancer

Sachan, Manisha; Kaur, Manpreet

doi:10.1590/s1516-8913201500132

Cited by 5 publications

(4 citation statements)

References 98 publications

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“…Other research groups have indicated the same profile [24–26]. A reduction in the cell count has also been obtained when procaine was combined with vorinostat in both concentrations, and similar profiles were obtained by other research groups [25, 27]. Meanwhile, in this combination, the dose has no significant effect, which might indicate the differences in the role of both procaine and vorinostat.…”

Section: Discussionsupporting

confidence: 71%

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Procaine Induces Epigenetic Changes in HCT116 Colon Cancer Cells

Sabit

Samy

Said

et al. 2016

Genetics Research International

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Colon cancer is the third most commonly diagnosed cancer in the world, and it is the major cause of morbidity and mortality throughout the world. The present study aimed at treating colon cancer cell line (HCT116) with different chemotherapeutic drug/drug combinations (procaine, vorinostat “SAHA,” sodium phenylbutyrate, erlotinib, and carboplatin). Two different final concentrations were applied: 3 μM and 5 μM. Trypan blue test was performed to assess the viability of the cell before and after being treated with the drugs. The data obtained showed that there was a significant decrease in the viability of cells after applying the chemotherapeutic drugs/drug combinations. Also, DNA fragmentation assay was carried out to study the effect of these drugs on the activation of apoptosis-mediated DNA degradation process. The results indicated that all the drugs/drug combinations had a severe effect on inducing DNA fragmentation. Global DNA methylation quantification was performed to identify the role of these drugs individually or in combination in hypo- or hypermethylating the CpG dinucleotide all over the genome of the HCT116 colon cancer cell line. Data obtained indicated that different combinations had different effects in reducing or increasing the level of methylation, which might indicate the effectiveness of combining drugs in treating colon cancer cells.

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Section: Discussionsupporting

confidence: 71%

“…Other mechanisms suggest the activation of caspase-activated DNase (CAD), which degrades DNA after a cascade of activation processes [38]. In the present investigation all drug combinations applied to HCT116 colon cancer cells have resulted in a degradation pattern that might indicate the occurrence of drugs-induced apoptosis [27, 39, 40]. …”

Section: Discussionmentioning

confidence: 89%

Procaine Induces Epigenetic Changes in HCT116 Colon Cancer Cells

Sabit

Samy

Said

et al. 2016

Genetics Research International

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“…The selected genes for this study were chosen because besides p53 loss-of-function by mutations, the epigenetic changes (DNA methylation, histones acetylation) regulated by p53 protein play a vital role in bladder cancer development (Lee et al, 2017;Sachan et al 2015). Therefore, the epigenetic role of the DNMT1, HAT1 and HDAC1 genes are directly involved on cell proliferation, cell cycle dysregulation or decreased cell death on bladder cancer (Porten et al 2018).…”

Section: Dnmt1 Hat1 and Hdac1 Gene Expressionmentioning

confidence: 99%

Chrysin inhibits the cell viability, induces apoptosis and modulates expression of genes related to epigenetic events in bladder cancer cells

Lima

Melo

Ferreira

et al. 2022

Natural Product Research

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This study was conducted with the aim of exploring the molecular and cellular mechanisms of action of the chrysin (natural flavonoid compound) on bladder tumour cell lines with different status of TP53 (RT4, 5637 and T24). The cells were treated with different concentrations of chrysin (20, 40, 60, 80 and 100 µM) to analyze the cell viability, nuclear division index, mutagenicity, apoptosis rates and expression of genes related to epigenetic events (DNMT1, HAT1 and HDAC1). Results showed that the treatment with chrysin reduced the cell viability and caused apoptosis, regardless TP53.Moreover, in the TP53-mutated cell lines, chrysin modulated the expression of the DNMT1, HAT1 and HDAC1 epigenetic genes, which might be a plus to the death observed in the cells with p53 mutation.

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“…Likewise, chromatin constituents can undergo covalent modifications, such as DNA methylation and post-translational modification of histone tails (Quina, Buschbeck, & Di Croce, 2006). The outcome of the cumulative modifications dictate the regions of the genome that will have access to the transcriptional machinery (Sachan & Kaur, 2015).…”

Section: Epigenetics: Looking At the Broader Imagementioning

confidence: 99%

Anti-neoplastic Effect of Adjuvant Epigenetic Therapy of Decitabine and Suberoylanilide Hydroxamic Acid on U937 Acute Myeloid Leukemia Cell Line. (c2020)

Babikian¹

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Acute myeloid leukemia is a heterogeneous malignant disorder characterized by rapid buildup of abnormal myeloid blasts in the blood and the bone marrow. This uncontrolled accumulation eventually interferes with the normal functioning of healthy blasts. Despite major advances in AML research, high incidence and death rates persist. Recently the role of epigenetic modifications in leukemogenesis has been well acknowledged, including histone deacetylation and DNA methylation, which frequently target the promoters of key genes involved in pathways such as apoptosis and cell cycle. Several studies have reported that combining different epigenetic modulators significantly boosts the effects of each one when used individually. In this study, the effects of a histone deacetylase inhibitor and a DNA methyl transferase inhibitor, suberoylanilide hydroxamic acid and Decitabine, respectively, were evaluated using U937 cells as an AML model cell line. Once having determined their growth inhibitory effects, and cell cycle arresting and apoptotic powers, two strategies of combining SAHA and DAC were assessed: simultaneous and sequential treatments. The sequential combination treatment, which consisted of priming the cells with DAC and then adding SAHA, was shown to enhance the effects of each epigenetic modulator, unlike the simultaneous treatment strategy. The effects were observed for growth inhibition, apoptosis stimulation and cell cycle arrest. Lastly, the changes incurred upon the sequential treatment were evaluated at the level of protein expression. The results revealed that, relative to controls and cells treated with only one drug, both intrinsic and extrinsic apoptotic pathways were activated by the sequential combination of SAHA and DAC. Further studies should be conducted to decipher the complete molecular mechanisms and pathways involved in the growth inhibitory effects of the combined SAHA and DAC treatment.

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Epigenetic Modifications: Therapeutic Potential in Cancer

Cited by 5 publications

References 98 publications

Procaine Induces Epigenetic Changes in HCT116 Colon Cancer Cells

Procaine Induces Epigenetic Changes in HCT116 Colon Cancer Cells

Chrysin inhibits the cell viability, induces apoptosis and modulates expression of genes related to epigenetic events in bladder cancer cells

Anti-neoplastic Effect of Adjuvant Epigenetic Therapy of Decitabine and Suberoylanilide Hydroxamic Acid on U937 Acute Myeloid Leukemia Cell Line. (c2020)

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