The research, in this article, is significant to human health because the understanding of the activity of a signal pathway can or cannot give you a grasp on how it can affect other processes in the body. If the effects are known and understood, then we can know how to treat and/or modify the processes and give a discovery in the field of science.
Specifically, in this article, understanding the structure of chromatin is vital to understanding how it affects replication, transcription, and repair. If DNA is not available for enzymes to carry out these processes, then genomic activity will not be as effective. Modifying histones is key to understanding the regulation of chromatin and its changes, and how it influences gene expression. Histone modification caused by an active NFκB signaling since it acts like a regulator for this modification can alter the tumor growth and furthermore give a resistance to chemotherapy. During the cisplatin-based treatment, an active NFκB signaling averts histone acetylation, which removes the positive charge from the histones making the condensed chromatin into a more relaxed structure (Ropero & Esteller, 2007). Therefore, there is histone deacetylation, which makes the chromatin in a more condensed and less relaxed structure, which will not allow transcription to take place or other processes that are needed for enzymes to carry them out.
Overall, understanding the structure of histones and how an active NFκB signaling will permit or prevent histone acetylation and deacetylation can affect tumor growth and can or cannot promote head and neck cell squamous carcinoma chemoresistance.
In this article, since it was found that treating head and neck squamous cell carcinoma with cisplatin-based chemotherapy demonstrated visible changes in the nucleus, the tumor cells were stained with Hoechest 33342 and immunofluorescence to distinguish the phenotype and were analyzed. (Almeida et al., 2014) It was seen that cells that were sensitive to cisplatin-based chemotherapy and normal cells had a massive increase in their nuclear size whereas cells that were resistant to the chemotherapy either had a decrease in their size or stayed in their original size (Almeida et al., 2014). Based on this, it was found that the reaction between the cells and cisplatin-based chemotherapy was caused by changes in the chromatin structure whether it was less condensed in a more relaxed structure or more condensed in a less relaxed structure.
It was also found that since chemoresistant cells have a smaller nucleus and less histone acetylation, creating histone acetylation and adding cisplatin in chemoresistant cells and chemosenstitive cells established that deacetylation and acetylation plays a part in the process. Next, it was determined if NFκB signaling plays a part in the condensation of chromatin whether it was active in chemoresistant cells and inoperative in chemosensitive cells. When NFκB was active in chemoresistant...