Transketolase attenuates the chemotherapy sensitivity of glioma cells by modulating R-loop formation
Fu et al. discover a non-metabolic function of TKT in gliomas. Mechanistically, TKT undergoes translocation from the cytoplasm to the nucleus following chemotherapy. Nuclear TKT interacts with XRN2 to prevent excessive R-loop accumulation, while depletion of TKT leads to increased R-loop accumulation and genome instability, potentiating chemotherapy efficacy.