1. Introduction
Background and Purpose
olorectal cancer is the third deadliest cancer in the world [1]. Cancer cells under different environmental conditions have different survival and proliferative power, resulting from successive mutations in the cancer cell [2]. Tumor formation is related to epigenetic changes in addition to genetic differences. One of the epigenetic pathways is histone acetylation. Acetylation opens the chromatin and allows the operator to access the transcription mechanism [3, 4].
Histone deacetylases are a group of enzymes responsible for removing acetyl groups from the amino acid lysine. Alterations of the histone deacetylase enzyme have been observed in many cancers, so drugs that inhibit this enzyme may play a role in inhibiting cancer [5]. Quisinostat as a new drug has high potential in the treatment of tumors [6]. It has anti-neoplastic properties in nanomolar doses by inhibiting the distillation of histones [7]. It has been suggested that epigenetic changes may be a sign of cancer diagnosis. These changes after transmission may play an essential role in cancer progression through gene transcription modulation, chromatin regeneration, and nuclear architecture. Alterations in acetylation or expression of HDAC have been associated with several solid tumor cancers [8].
2. Materials and Methods 
Quizinostat was dissolved in DMSO, which is a natural analgesic and anti-inflammatory. To dissolve the drug, a safe amount was calculated. Three groups were considered for the experiment, respectively. The first group was untreated cells, the second group was cells treated with quizinostat with a concentration of 200 nM, and the third group was cells treated with DMSO.
The cell suspension was cultured in the upper wells of the Boyden chamber assay, where 1000 cells with 50 μL of culture medium were placed in each well.
Cells migrate along the membrane. Since quisinostat is dissolved in DMSO, and due to the toxicity of DMSO for cells, it was calculated that the concentration of DMSO in the well should not exceed 0.25%. To investigate the migration of treated cells to the lower wells, 225 μL of culture medium was poured into each well. This experiment was measured 24 hours after treatment and repeated 3 times. To count the migration rate 24 hours after treatment, the lower part was stained with a fluorescent dye, and the number of cells in the lower well was measured with a special microscope.
3. Results
Before adding the cell suspension to the upper part of the cell membrane, they were kept in a culture medium without FBS for 24 hours until they reached starvation. 24 hours later, the number of cells migrating to the lower abdomen was counted. It should be noted that according to the cell size, the size of 12 μM well filter holes was selected [10]. The results showed that quisinostat is a beneficial and effective drug to prevent the migration of cancer cells and prevent metastasis and spread of cancer in the long run. The figure shows that treatment of cells with quisinostat nM200 reduced cell migration by 50% (Figure 1).  Treatment was assessed 24 hours after cell culture and 24 hours after treatment by cell fluorescence microscopy. All experiments were repeated at least 3 times. Data were analyzed using a one-way ANOVA test. In this test, a value of 0.05 or less was considered significant.
4. Discussion and Conclusion
In this paper, treatment with HDACi on colorectal cell lines was investigated. The results showed that DMSO alone did not significantly affect cell migration, but treatment with quisinostat reduced the migration rate by up to 50%. It can be concluded that quisinostat by histone distillation has caused chromatin compression and subsequent suppression of genes effective in the expression of proteins necessary for cell migration [8]. Previous research has also evaluated the effect of HDACi on proliferative cell pathways in cancer and found, for example, that HDACi can activate P53 [5] or increase the susceptibility of cancer cells to apoptosis [4]. Oral administration of quisinostat causes persistent H3 acetylation and inhibits tumor progression in colorectal tumors [3].
The histone deacetylase enzyme affects chromatin by deacetylating lysine residues; it restricts histones available at transcription sites. The adverse activity of this enzyme has been observed in a variety of cancers. This activity transforms cancer cells into CSCs and increases metastasis and cell migration because it prevents the expression of genes that lead to defective cells leading to apoptosis [9, 11]. Members of the distilling enzyme family have played a vital role in the development and progression of cancer. In recent years, by examining the expression of the gene that produces these enzymes in various types of cancer and the effect of inhibitory drugs, it has been possible to create therapeutic goals, especially new medicines in the treatment of cancers [4].
Investigation and repair of histone acetylation can play an essential role in the homeostasis and function of chromatin proteins; these molecules inhibit its function by binding zinc ions in the active site of the deacetylating enzyme [8]. Also, during the use of HDACi, this drug has an influential role in killing cancer cells due to the greater sensitivity of cancer cells to apoptosis than normal cells [8, 12]. This study showed that quisinostat, as a histone acetylation inhibitor, could inhibit cell migration and prevent cancer metastasis.

Ethical Considerations
Compliance with ethical guidelines
This study was the result of a preliminary study of Shiraz University (Code: 96GCU3M1293).

Funding
This research did not receive any grant from funding agencies in the public, commercial, or non-profit sectors. 

Authors' contributions
All authors met the standard writing standards based on the recommendations of the International Committee of Medical Journal Publishers. 

Conflicts of interest
The authors declared no conflict of interest.

Acknowledgements
The authors would like to thank the Rome Health Research Center of Italy and the esteemed colleagues in the Biobank Center for their help in implementing this project.


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