ANGPTL4 and neoplasm: Furthermore, we validated that the knockdown of ANGPTL4 could markedly inhibit the D-2HG-induced activation of the integrin and downstream pathways (Fig. 5E) and also confirmed that ANGPTL4 knockdown mitigated the effect of D-2HG on cell cycle progression and EMT process in TNBC cells (Fig. 5F), suggesting that D-2HG-induced ANGPTL4 could bind to integrin proteins in TNBC tumor cells and activate a series of downstream oncogenic signaling pathways, thus promoting TNBC progression.