Abstract
Cervical cancer outcomes remain suboptimal, underscoring the need to define molecular drivers that can be therapeutically exploited. Insulin-like growth factor 2 mRNA-binding protein 3 (IMP3) has been implicated in tumor biology, but its role in cellular metabolism is not well characterized. Here, we investigate the metabolic consequences of IMP3 suppression in HeLa cells and integrate these findings with transcriptomic analyses of clinical datasets. siRNA-mediated knockdown of IMP3 reduced mitochondrial oxygen consumption rate and altered cellular energy status, as evidenced by changes in ATP/ADP and NADP+/NADPH ratios, alongside shifts in key intermediary metabolites. Complementary bioinformatic analyses of Gene Expression Omnibus datasets revealed that cervical cancers with high IMP3 expression exhibit coordinated deregulation of metabolic, cell-cycle, and inflammatory response pathways relative to normal cervical tissue. Consistent with these signatures, IMP3 silencing produced pronounced effects on lipid metabolic readouts in vitro. Together, these data identify IMP3 as a regulator of energy and lipid metabolism in cervical cancer and support its evaluation as a biomarker and potential therapeutic target.