Membranous Met is classically identified with its role in cancer metastases,
while nuclear Met is associated with a more invasive, aggressive and proliferative
form of cancer. Full-length Met or N-terminal transmembrane domain
cleaved Met can translocate into nucleus in a cell growth and pH dependent but
both ligand-dependent (full length Met) and -independent (cleaved Met) manner.
nMET may play greater essential roles in cancer recurrence than membranous
Met. For example, in prostate cancer, it has been found that androgen receptor
(AR) may inhibit the expression of membranous Met so anti-androgen based prostate
cancer therapy may promote the expression of nuclear Met (nMET). We recently
found a novel nMET/SOX9/ β-Catenin/AR pathway in relapsed prostate
cancer which may contribute to the formation of the feedback loop of AR reactivation via
MET/nMET. Emerging evidence suggests the possibility of nMET as a prognostic marker in relapsed
cancer. This review summarizes recent findings about nMET and its unique role in recurrent cancer.
Keywords: Met, nuclear translocation, oncogene, recurrence.
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