Abstract
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.
Highlights
Cancer, the uncontrolled cell growth, is one of the most fatal diseases worldwide [1]
Trypan blue assay was performed to assess the cell viability after treatment with the chemotherapeutic drug/drugs combinations as it can stain the dead cells while leaving the viable cells unstained
Results obtained showed that there was a significant decrease in the cell viability after being treated with different concentrations/combinations of the chemotherapeutics under study (Figures 1 and 2 and Table 3) (P < 0.01)
Summary
The uncontrolled cell growth, is one of the most fatal diseases worldwide [1]. It is well known that epigenetic alterations, in the disease-related genes, are associated with various disorders including many cancer types [5]. Colorectal carcinoma is one of those diseases in which epigenetic inactivation of multiple tumor suppressor genes plays a crucial role in the tumorigenesis process [6]. The role of DNA methylation in the organization of the cancer epigenetic profile is still unclear. Several studies have been conducted on HCT116 colon cancer cells to elucidate the landscape of DNA methylation [7, 8]
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