HADHA promotes esophageal cancer progression by activating mTOR signaling and the SP1/MDM2 axis

• HADHA is significantly upregulated in esophageal cancer tissues and correlates with poor patient survival. • Knockdown of HADHA inhibits EC cell proliferation, induces apoptosis, causes cell cycle arrest, and suppresses migration in vitro and in vivo. • HADHA activates mTOR signaling and interacts with SP1 to induce MDM2 expression, revealing a novel oncogenic mechanism. • Targeting HADHA or its downstream pathways (mTOR and SP1/MDM2) may offer new therapeutic strategies for esophageal cancer.