STTT：中南大学袁霞/周艳宏合作发现结直肠癌治疗新靶点——INHBA

Core Viewpoint - Colorectal cancer (CRC) remains a significant health challenge globally, with high incidence and mortality rates, necessitating further research into molecular mechanisms and potential therapeutic targets [1][2]. Group 1: Research Findings - The study published in Signal Transduction and Targeted Therapy indicates that Inhibin beta A (INHBA) drives CRC progression by reprogramming tumor-associated macrophages (TAM) to the M2 phenotype and suppressing mitochondria-dependent ferroptosis in CRC cells [2][7]. - Elevated INHBA expression in CRC tissues correlates with poor clinical outcomes, promoting cancer cell growth, migration, and invasion, while silencing INHBA inhibits these malignant behaviors [5][7]. - Mechanistically, INHBA activates the succinate/SUCNR1 signaling axis by upregulating SLC25A10, promoting M2-like TAM polarization, and inhibits ferroptosis in CRC cells through the mitochondrial glutathione/GPX4 pathway [5][7]. Group 2: Implications for Treatment - The findings provide a theoretical basis for developing INHBA-targeted inhibitors or combined immunotherapy strategies that induce ferroptosis, potentially improving CRC treatment outcomes [2][7].