Introduction: Unlimited mitosis is the main fact behind the concept of cancer cell proliferation. Disruption of the mitotic division process makes the tumor cells undergo mitotic arrest. Generally, it is followed by the death of the above-mentioned cells. Antimitotic therapy has been identified as an effective and essential way of treating cancer. It is noteworthy that there are several libraries in which lots of anti-mitotic agents are introduced for further scientific research. In order to apprehend the antitumor mechanism of such chemicals, one bioactive compound, MT7, has been chosen as a model. In previous research which was done by Zhang et al., Microarrays results of HeLa cells in a time period of MT7 treatment were published. The gene expression profiles were further analyzed by Functional Protein Association Networks.
Methods: A dataset containing 5 samples was retrieved from NCBI and its heat map was drawn. Firstly, the part of the heat map which has the highest contrast between the control sample and 12 hours treated one was selected and corresponding genes were analyzed in String package and their Functional Protein Association Networks were drawn. Secondly, the table of genes ordered by significance has been extracted from GEO2R and its related Networks on 1300 major contributing genes were analyzed by String package.
Results: It can be concluded that cell proliferating limitation which was the result of treating cell culture by MT7 is not just because of mitotic arrest. There is another mechanism called cellular senescence which is acting as a great factor in limiting cancer cell proliferation in a synergic way.
The results somehow illuminate the role of MT7 compound in mitotic arrest and it is expected to be regulating checkpoints of cell cycle and not allowing the cells to go further in the cycle.
Conclusion: By and large, MT7 restricts cancer cells’ division in several mechanisms. As it was discovered before, it makes cancer cells undergo mitotic arrest. By analyzing the network which was mentioned before, it seems that it also helps the process of stopping cell proliferation in several other ways like “cellular senescence”. Its role in the regulation of cell cycle checkpoints is of much importance and there is a need to understand more about this pathway.