n-3 Polyunsaturated fatty acids induce acute myeloid leukemia cell death associated with mitochondrial glycolytic switch and Nrf2 pathway activation

Human hematopoietic stem/progenitor cells display reactive oxygen species-dependent long-term hematopoietic defects after exposure to low doses of ionizing radiations

“…As increased ROS levels can lead to 8-oxo-dG lesions, as well as NRF2 translocation into the nucleus, we looked for 8-oxo-dG lesions in DNA of irradiated versus sham-irradiated HSPC 30 , 31 and NRF2 location into HSPC. 22 , 24 As expected sham-irradiated and H 2 O 2 -treated (control) cells exhibited respectively no and highly detectable anti-8-oxo-dG nuclear labeling. After exposure to 20 mGy, 8-oxo-dG staining was detected in the HSPC nucleus showing that 20 mGy LDIR can induce 8-oxo-dG lesions in DNA ( Figure 5B and C ).…”

“…Immunofluorescence was performed on cell-sorted HSPC irradiated and incubated 30 min, 1 hour (h), or 3 h at 37°C in MyeloCult medium, as previously described. 22 – 24 Details of the methods used are available in the Online Supplementary Methods .…”

Disruption of gap junctions attenuates acute myeloid leukemia chemoresistance induced by bone marrow mesenchymal stromal cells

“…Since CBX showed antileukemic activity, we investigated the combination effect of CBX and the antileukemic agent Ara-C by isobologram analyses. To this end, individual IC 50 doses for CBX and Ara-C were determined and then plotted on the x and y axes, according to method previously described [38]. The isobolograms of AML cell lines showed a synergistic effect between the two drugs ( Supplementary Fig.…”

“…Human AML cell lines were purchased from the European Collection of Authenticated Cell Cultures (ECACC, Wiltshire, UK) and cultured as previously described [38]. The FILOtheque AML (# BB-0033-00073, Cochin hospital, Paris, France), tumor bank of the FILO (French Innovative Leukemia Organization) group, provided 39 annotated samples.…”

Therapeutic Effects of Specialized Pro-Resolving Lipids Mediators on Cardiac Fibrosis via NRF2 Activation

“…N-3 PUFA induces inflammatory resistance through the formation of KEAP1-containing cytosolic speckles of the autophagic receptor SQSTM1/p62 (sequestosome 1) SQSTM1/p62-body and activation of NFE2L2 [151]. n-3 PUFA induces acute myeloid leukaemia cell death associated with mitochondrial glycolytic switch from oxidative respiration and the activation of the NRF2 pathway [152]. EPA treatment also increased NRF2 nuclear translocation and antioxidant activity, leading to the upregulation of HO-1 expression, and treatment with EPA reduced apoptosis due to hydrogen peroxide [153].…”