Fig. 7

Illustration of the potential mechanisms by which AKR1B10 induces PEM chemotherapeutic resistance in lung cancer brain metastasis. In brain metastatic lung cancer cells, elevated AKR1B10 promotes glycolysis through upregulating the expression of LDHA and the resulting increased lactate induces transcriptional activation of the cell cycle-related gene CCNB1 by histone lactylation, leading to the chemotherapeutic resistance to PEM.