Peptide G-Protein-Coupled Receptors and ErbB Receptor Tyrosine Kinases in Cancer

The ErbB RTKs (EGFR, HER2, HER3, and HER4) have been well-studied in cancer. EGFR, HER3 stimulate cancer proliferation, principally by activating the phosphatidylinositol-3-kinase extracellular signal-regulated kinase (ERK) pathways, resulting increased cell survival proliferation. Cancer cells high densities of causing phosphorylation tyrosine amino acids on protein substrates near C-terminal RTKs. After transforming growth factor (TGF) α binds to homodimers or EGFR heterodimers form. HER2 forms with HER4. are overexpressed lung patient tumors, monoclonal antibodies (mAbs), such as Herceptin against used treat breast patients. Patients mutations treated inhibitors, gefitinib osimertinib. Peptide GPCRs, NTSR1, present many cancers, neurotensin (NTS) stimulates cells. Lung proliferation is impaired SR48692, an NTSR1 antagonist. SR48692 synergistic at inhibiting growth. Adding NTS increases shedding TGFα, which activates neuregulin-1, HER3. transactivation process SRC, matrix metalloprotease, reactive oxygen species inhibitors. While complicated, it fast occurs within minutes after adding This review emphasizes use inhibitors impair