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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Animals, Antineoplastic Agents, Cell Movement, Cytoskeletal Proteins, Drug Resistance, Neoplasm, Ephrin-B2, Female, Humans, Imatinib Mesylate, K562 Cells, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Mice, Mice, Nude, Phosphorylation, Receptor, EphB4, Xenograft Model Antitumor Assays, cdc42 GTP-Binding Protein, rac1 GTP-Binding Protein, rhoA GTP-Binding Protein.
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Does ephB4/ephrinB2 contribute to Imatinib Resistance in Chronic Myeloid Leukemia Involved in Cytoskeletal Proteins? Context: The mechanism of EphB4/ephrinB2 in the resistance of chronic myelogenous leukemia to imatinib keeps unknown. The imatinib resistant chronic myelogenous leukemia cell line-K562-R, was established. EphB4 receptor expression was detected in patients and resistant cells. Cell migration and drug sensitivity were tested in the EphB4 knockdown cells and mouse models. The EphB4 receptor was over-expressed in blast crisis patients compared to chronic phase patients. The level of EphB4 receptor expression was associated with a complete cytogenetic response within 12 months. Enhanced expression of the EphB4 receptor was detected in the K562-R cells. EphB4 knockdown inhibited cell migration ability and restored sensitivity to imatinib in vitro and in vivo. Restored sensitivity to imatinib was observed in K562-R cells, along with increased levels of phospho-EphB4 and decreased phosphorylation levels of RhoA, Rac1, and Cdc42.
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Our study illustrates that aberrant activation of EphB4/ephrinB2 may mediate chronic myeloid leukemia resistance involved in cytoskeletal proteins. Final Decision: yes