Receptor Tyrosine Kinase Activation in Cancer Cells
The aberrant activation of RTKs is a complex process that not only involves the RTKs but also their partner molecules and environment. The mechanisms of oncogenic RTK activation are further complicated by their connection with several subgroups of cellular components. The following four primary pathways have been put up as causes of abnormal activation:
- Increased RTK expression
- Mutations that increase function
- Chromosomal translocations
- Autocrine activation.
Along with these fundamental pathways, other factors that can affect oncogenic RTK activation include kinase domain duplications, microRNAs, alterations in the tumour microenvironment, protein tyrosine phosphatases, altered endocytic/trafficking genes, and geographic dysregulation of RTKs.
Receptor Tyrosine Kinase Signaling
Cell signalling is a cell’s capacity to accept, process, and transmit messages to its surroundings and to itself. Cell signalling is a basic characteristic of all prokaryotic and eukaryotic cellular life. Extracellular signals (or signals that originate outside of a cell) can be physical agents such as mechanical pressure, electricity, temperature, light, or chemical signals (e.g., small molecules, peptides, or gas).