The researchers found this particular protein, called H2A.Z.2, acts to promote the abnormal growth characteristics of melanoma cells when they develop into more advanced stages of difficult-to-treat tumors. H2A.Z.2 is part of the chromosomal structure that packages genes and has the power to switch certain genes on and off. Upon high levels of this protein, there is an abnormal activation of several growth-promoting genes within melanoma cells.
There is a recent theory surrounding cancer that states that abnormal growth might result not only from unlucky mutations that occur randomly in patients’ genes but also from some genes being turned on and off as a consequence of epigenetic mechanisms. The authors managed to found that blocking H2A.Z.2 functions using targeted methods or in combination with cancer therapies, could effectively block tumor growth and kill melanoma cells.
“Cancer is a disease consisting of both genetic and epigenetic changes. I believe that the study of epigenetic mechanisms may lead to the development of new approaches for molecular diagnosis and targeted treatments,” said the study lead author Emily Bernstein, PhD, Associate Professor of Oncological Sciences and Dermatology, the Icahn School of Medicine at Mount Sinai.
Dr. Bernstein added, “Here we show that the histone variant H2A.Z.2 drives melanoma progression by affecting chromatin structure. This is the first study to identify a specific role for the histone variant H2A.Z.2 in any tumor type. Next, we need to better understand how to prevent H2A.Z.2 function in chromatin.”
According to Dr. Bernstein, this research has only cleared some of the epigenetic mechanisms involved in cancer. Further knowledge on the mechanisms behind these phenomenons will allow researchers to design new and innovative therapeutic regimens not only for melanoma but also for other types of cancer.