Lipid overload-induced DNA double stands breaks foci in HCC genome

Lipotoxicity-induced hepatic DNA damage responses (DDRs) contribute to malignant progression of MASH-related HCC, but the underlying mechanism is unclear. Using DSB marker phosphorylation of the Ser139 residue of the histone variant H2AX (?H2AX) antiby-mediated CUT&Tag-seq, a global increase of DSBs induced by PA+OA was observed. Overall design: Using DSB marker phosphorylation of the Ser139 residue of the histone variant H2AX (?H2AX) antibody-mediated CUT&Tag-seq to reveal a global of DSBs foci in lipid overload-induced or mock-induced HepG2 cells