
Frontiers in Immunology, Год журнала: 2024, Номер 15
Опубликована: Ноя. 27, 2024
Cellular mesenchymal-epithelial transition factor (c-MET), also known as hepatocyte growth receptor (HGFR), is a crucial tyrosine kinase implicated in various solid tumors, including lung, breast, and liver cancers. The concomitant expression of c-MET PD-L1 such hepatocellular carcinoma, highlights their prognostic significance connection to therapeutic resistance. Cancer-associated fibroblasts mesenchymal stromal cells produce (HGF), activating signaling tumor myeloid-derived suppressor (MDSC). This activation leads metabolic reprogramming increased activity enzymes like glutaminase (GLS), indoleamine 2,3-dioxygenase (IDO), arginase 1 (ARG1), depleting essential amino acids the microenvironment that are vital for effector immune cell function. review interplay between (MDSCs) create an immunosuppressive environment while providing targets c-MET-focused immunotherapy. It emphasizes clinical implications inhibition on behavior neutrophils, macrophages, T cells, NK cells. explores potential antagonism combined with immunotherapeutic strategies enhance cancer treatment paradigms. discusses innovative immunotherapies targeting c-MET, chimeric antigen (CAR) therapies, monoclonal antibodies, antibody-drug conjugates, encouraging development comprehensive strategy simultaneously tackles evasion enhances anti-tumor efficacy further improve prognoses patients c-MET-positive malignancies. Despite challenges variability across different subtypes, continued research into molecular mechanisms will be crucial.
Язык: Английский