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CBL encodes E3 ubibin connective enzymes and signal transducting joints that regulate the conductor and non-receivable tyrosine kinase.
reococculative CBL mutation selectively destroys the E3 ubibin connective enzyme activity of proteins, occurring in myelin tumors, including 10-20% chronic granulocyte monocytoblast leukemia (CMML).
the CBL mutation is related to the patient's poor prognostication, but the carcinogenic mechanism of the CBL mutation and the significance of treatment are not completely clear.
, such as Belizaire, combine functional detection and overall mass spectrometry to define phosphate proteomics, CBL interaction groups, and signal activation mechanisms in a cell line that expresses all-like gene mutations.
CBL functional accessibility mutation and lecithin sensitivity and LYN and PI3K/AKT activation enhancement related to LYN promote CBL-PIK3R1 interaction, enhance the proliferation of CBL mutant cells The study analysis shows that LYN activation enhancement and interaction with mutant CBL are the key drivers of CBL phosphate enhancement, PIK3R1 collection and downstream PI3K/AKT signal transmission in CBL mutant cells.
CBL signal convergence substructors, including tyrosine kinase binding domain, proline-rich areas and C-end tyrosine phosphate site, are necessary for CBL mutations to perform cancer-causing functions.
dasatinib inhibits the proliferation of CBL mutant cells, CBL phosphorylation, PI3K/AKT signals, and CBL-PIK3R1 mutual genetic ablation and dasatinib-mediated LYN inhibition reduces CBL phosphorylation, CBL-PIK3R1 interactions, and PI3K/AKT signals.
addition, the researchers also confirmed that dasatinib has anti-proliferation activity in both CBL mutant cell line and primary CMML, both in vivo and in vitro.
, the analysis of the molecular mechanism of CBL mutation provides a theoretical basis for exploring the therapeutic potential of LYN inhibition in CBL mutant myelin-like malignancies
