Acceleration of slow autophagy flux induced by arabinofuranosyl cytidine improves its antileukemic effectiveness in M-NFS-60 cells

Arabinofuranosyl cytidine (AraC) is an analog of deoxycytidine used as anticancer drug for leukemic patients. The effective dose always produces severe complications. present study investigated the modulation autophagy and its impact on cytotoxicity AraC toward murine myelogenous leukemia cells (M-NFS-60). Autophagy was inhibited by NH4Cl or Bafilomycin A1 enhanced amino acid starvation, glucose mild hyperthermia (41 °C), rapamycin (Rap). Cells were treated with different concentrations, 0 to 2 µM, in presence absence modulators. AraC-induced apoptosis combined autophagy, especially at lower concentrations. This characterized a slow flux, indicated levels LC3B II P62 proteins. Inhibition did not alter cleaved caspase 3 (c-casp.3) cell viability measured MTT assays. Conversely, acceleration co-treatment inducers reduced increased c-casp.3 c-PARP levels. Further, inhibitor, Z-VAD-FMK. Enhancement autophagic flux induced low concentrations significantly M-NFS-60 cells. Such coadministration might improve efficacy treatment reduce doses.