Overall, these findings suggest that downregulation of miR-3127-5p promotes EMT through activating the Wnt/FZD4/β-catenin signaling pathway and may represent a therapeutic target for NSCLC metastasis.
Finally, a reduction was observed in the expression of integrin α5 (ITGA5) upon heterodimerization, supported by decreased cell adhesion to extracellular matrices <i>in vitro</i> Taken together, the data identify a novel pharmacologic mechanism for the modulation of tumor cell migration and invasion in the context of metastatic disease.<b>Implications:</b> This study investigates a signaling mechanism by which GPCR heterodimerization inhibits cancer cell migration.<i></i>.
This review focuses on the recent report of a mouse melanoma model, TG-3, which has implicated the ectopic expression of the metabotropic glutamate receptor 1 (Grm1), a G protein coupled receptor (GPCR), in melanomagenesis and metastasis.
Protease-activated receptor 1 (PAR1), a thrombin-responsive G protein-coupled receptor (GPCR), is implicated in promoting metastasis in multiple tumor types, including both sarcomas and carcinomas, but the molecular mechanisms responsible remain largely unknown.
Notably, HRG treatment upregulates surface expression levels of CXCR4, a G protein-coupled receptor (GPCR) implicated in breast cancer metastasis and an indicator of poor prognosis in breast cancer patients.
Signaling activated by binding of the C<i>X</i>C motif chemokine ligand 12 (CXCL12) to its cognate G protein-coupled receptor (GPCR), chemokine C<i>X</i>C motif receptor 4 (CXCR4), is linked to metastatic disease.