Research has shown faulty or mutated versions of MET to be involved in cancer cell growth and spread in a variety of cancer types; however, the precise mechanisms by which it controls these processes are unknown.
MET belongs to a group of proteins called receptor tyrosine kinases (RTKs), which are key regulatory proteins involved in a variety of signaling pathways that control normal cellular processes. Abnormal changes to RTKs are implicated in the development and progression of many types of cancer, making them a popular target for cancer treatment.
They found that the protein activated two distinct pathways to drive cancer cell growth and migration, by interacting with other key molecules that help MET to carry out these functions.
One molecule identified as a key player in these MET-driven processes was Rac1. It is widely understood that Rac1 is involved in cancer cell migration; however, the team found Rac1 to also be critical in driving cancer cell growth, via interaction with another protein called mTOR. This interaction occurs inside the cells (in structures called endosomes), followed by a relocation of the two molecules to the cell boundary—an unusual place for mTOR to be found. In a separate pathway, MET also communicates with another molecule, PI3K, to drive cell migration.
reference
A PI3K- and GTPase-independent Rac1-mTOR mechanism mediates MET-driven anchorage-independent cell growth but not migration, Science Signaling, 23 Jun 2020: Vol. 13, Issue 637, eaba8627, DOI: 10.1126/scisignal.aba8627 , stke.sciencemag.org/content/13/637/eaba8627
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