AIM: To investigate the effect of c-Myc inhibitor 10058-F4 on human chronic myeloid leukemia ( CML) K562 cells and imatinib-resistant K562/G cells.METHODS: The protein expression of c-Myc was detected by Western blotting .Cell proliferation was evaluated by MTT assay and colony formation assay .PI staining was used to deter-mine the cell cycle distribution .Annexin V-PI staining was applied for apoptosis detection .RESULTS:Imatinib-resistant K562/G cells displayed lower sensitivity to imatinib than K 562 cells with high expression of c-Myc.Treatment with specific c-Myc inhibitor 10058-F4 inhibited the cell proliferation in a dose-and time-dependent manner , and K562/G displayed more sensitivity to 10058-F4 than K562 cells.10058-F4 also induced cell cycle arrest in G 0/G1 phase and induced apoptot-ic cell death in the 2 cells.Importantly, 10058-F4 suppressed the colony formation ability in K 562 and K562/G cells. CONCLUSION:c-Myc is a novel target to overcome imatinib-induced drug resistance , and c-Myc inhibitor provides a new approach in CML therapy .

Both chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea syndrome (OSA) are common respiratory diseases. Both can exist at the same time, which is referred to as the " overlap syndrome (OS)". Epidemiological studies showed poorer outcomes with increased comorbidities and mortality, which indicated complicated interactions between COPD and OSA. Even though the underlying mechanisms of overlap syndrome have not yet well understood, the airway and systemic inflammation as well as oxidative stress induced by hypoxia played an essential role in the disease interactions and pathogeneses of comorbidities, mainly cardiovascular diseases. One other question is that how to treat the overlap syndrome. This paper summarizes the current research progress of the overlapping interaction and treatment.