The researchers analyzed 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, published in the journal Cell Death & Disease, indicates that a dysfunctional relationship between the Smad7 and β-catenin complex can lead to a situation of impaired muscle cell differentiation -- a hallmark of some soft tissue cancers such as Rhabdomyosarcoma (RMS). This 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.
Cells - Muscle - Character - Difference - Muscle
"What happens in those rhabdomyosarcoma cells is that they have a muscle cell-like character, but the difference is that normal muscle cells stop dividing," said John McDermott, a professor in the Department of Biology in the Faculty of Science, who supervised the study and is a contributing author.
McDermott said these cells look like muscle cells, in terms of the way they function and their phenotype, but they don't stop dividing, which is why they form tumors at various sites in the body.
Idea - Part - Reason - Cells - Differentiation
"Our idea is that part of the reason why those cells are defective in the differentiation program, which would mean that they would stop dividing, is that the β-catenin complex is being degraded in those cells because of an anomaly in the signaling pathway that controls that," said McDermott. "If we can stabilize the β-catenin and Smad7 complex in those cells, you could potentially encourage them to differentiate and stop proliferating, which would mean that you'd stop those...
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