Furthermore, we show that targeting mitochondrial metabolism, particularly by inhibiting Complex I, sensitizes CRC cells to 5FU, resulting in delayed tumour growth and prolonged survival in preclinical models
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In the face of controversies and challenges, it is essential to establish a more efficient translational interface between science, technology, and clinical practice, driving mitochondrial metabolic reprogramming therapy from a potential pathway to clinical reality. Conclusion Mitochondrial metabolic reprogramming plays a central role in the therapeutic failure of CRC
