HDAC9/p300/F-actin immunoexpression and migration analysis for malignant melanoma stem cell

Melanoma is an aggressive tumor with a poor prognosis that worsens in the metastatic phase. Distruptions of epigenetic mechanisms is known to effect cancer stem cells (CSCs) activity. Malignant melanoma (MM) progression may be promoted by changes in the genetic structure of CSC. Thus, treatments that target epigenetic modifications could be a promising weapon, especially in melanoma. Here, we compared p300, HDAC9, and Factin proteins in melanoma CSCs (CD133+), non-CSCs (CD133-) and CHL-1 cell line, as well as cell migration and division rates. At 4 and 6 h, P300 protein levels in CHL-1 and CD133 + were remarkably similar, and the CD133- showed increases in expression levels as the incubation period lengthened. HDAC9 protein intensity decreased in CHL-1, increased in the CD133-, and remained relatively unchanged in the CD133+ as the incubation period lengthened. The mean value of F-actin expression level increased in all cell group with time, when the highest increase observed in CHL-1. In conclusion, our studies contribute to the management of metastatic diseases in the future and offer new insight into the molecular basis of the initiation and progression of MM.

Automated summary

Melanoma is a highly aggressive tumor with poor prognosis that can worsen during the metastatic phase. This study investigates the role of epigenetic mechanisms and cancer stem cells in melanoma progression, and suggests that targeting epigenetic modifications may be a promising treatment strategy. The study compares the levels of p300, HDAC9, and Factin proteins in different cell populations and explores their association with cell migration and division rates. The findings shed light on the molecular basis of melanoma initiation and progression, and contribute to the future management of metastatic diseases.