Apigenin Inhibits Triple‐Negative Breast Cancer Growth by Dual Targeting <scp>GPX4</scp> / <scp>SLC7A11</scp> ‐Mediated Ferroptosis and <scp>PKM2</scp> / <scp>GLUT1</scp> ‐Mediated Aerobic Glycolysis

, MDA, and ROS levels while decreasing reduced GSH levels, downregulated GPX4, SLC7A11, FPN1, FTH1, FTL, and FSP1 expression, and upregulated TFR expression, indicating ferroptosis induction. API also decreased lactic acid, ATP, and ECAR levels while increasing intracellular glucose and OCR levels, downregulating PKM2, GLUT1, GLUT4, HK2, and LDHA expression, demonstrating glycolysis inhibition. In vivo, API significantly inhibited tumor growth in the 4T1 xenograft model without obvious toxicity and regulated the expression of ferroptosis and glycolysis-related proteins. These findings establish API as a promising natural anti-TNBC drug by simultaneously targeting ferroptosis and aerobic glycolysis.