York University scientists have discovered a unique set of genes in muscle cellular gene expression and differentiation that could lead to new therapeutic targets to prevent the spread of muscle cancer.
The researchers analysed gene networks in muscle cells and found that the Smad7 and β-catenin proteins work cooperatively inside the body to regulate muscle cell differentiation, growth and repair.
When these regulatory proteins work in harmony, they control the pathway for normal gene expression, resulting in normal skeletal muscle cells.
The study indicates that the dysfunctional relationship between the Smad7 and β-catenin can cause an impaired muscle cell differentiation which leads to soft tissue cancers such as Rhabdomyosarcoma (RMS).
Rhabdomyosarcoma (RMS) is rare cancer, which most often affects children, forms in soft tissue, mostly skeletal muscle tissue, and sometimes in hollow organs like the bladder or uterus.
Rhabdomyosarcoma cell looks, functions and their phenotype is similar to that of the muscle gene cell, as they don't divide from the muscle cells they form tumours.
The β-catenin complex is being degraded in rhabdomyosarcoma cells because of an anomaly in the signalling pathway that controls and holds the cells from dividing.
York scientist said stabilising the β-catenin and Smad7 complex in those cells, could potentially differentiate and stop proliferating, which would stop those cells from growing in the tumour.
The research team focused on understanding the role of transcription factors in orchestrating tissue-specific gene expression and differentiation. By identifying DNA binding proteins that are involved in transcriptional regulation during muscle development.
They also identified new regulators in muscle regeneration which can open doors for the pharmaceutical industry to develop new treatments to treat debilitating loss of muscle in the ageing population.
