Hypoxia facilitates triple-negative breast cancer stem cells enrichment and stemness maintenance through oxidized ataxia telangiectasia mutated-induced one-carbon metabolism

Figure 1 Hypoxia promotes enrichment and DNA damage-independent oxidative activation of ataxia telangiectasia mutated. A: Flow cytometry analysis of CD44+/CD24- cell populations in Hs578T and MDA-MB-231 cells after exposure to hypoxia or normoxia; B: Quantitative reverse transcriptase polymerase chain reaction analysis of cancer stem cells-associated genes (c-Myc, octamer-binding protein 4, Kruppel-like factor 4, sex-determining region Y-box 2, NANOG) in mammosphere cultures under hypoxia; C-E: Western blot analysis of phosphorylated ataxia telangiectasia mutated, γH2AX, and 53BP1 in Hs578T and MDA-MB-231 cancer stem cells under normoxia, hypoxia, or H₂O₂ treatment. Data were presented as mean ± SD (n = 3). ^aP < 0.05; ^bP < 0.01; ns: not significant. KLF4: Kruppel-like factor 4; SOX2: Sex-determining region Y-box 2; OCT4: Octamer-binding protein 4; p-ATM: Phosphorylated ataxia telangiectasia mutated.