AI Article Synopsis
- Drug resistance in cancer chemotherapy is a major issue, with cancer cells often shifting to fatty acid metabolism to evade treatment.
- The researchers created a drug called folate-polySia (FpSA) that induces microcalcification in cervical cancer cells resistant to cisplatin, leading to decreased fatty acid uptake and increased glycolysis.
- The combination of cisplatin and FpSA not only inhibited tumor growth but also improved survival rates in mice, suggesting a new strategy to tackle chemotherapy-resistant tumors by reprogramming cancer cell metabolism.
Article Abstract
Drug resistance is an inherent challenge during cancer chemotherapy. Cancer cells favor fatty acid metabolism through metabolic reprogramming to achieve therapeutic resistance. However, an effective approach to overcoming the switch from glycolysis-dependent to fatty acid beta-oxidation-dependent anabolic and energy metabolism remains elusive. Here, we developed a macromolecular drug (folate-polySia, FpSA) to induce the extracellular microcalcification of cervical cancer cells with cisplatin resistance. Microcalcification attenuated the uptake of fatty acids and the beta-oxidation of fatty acids by mitochondrial dysfunction but boosted the glycolysis pathway. Consequently, cotreatment with Pt and FpSA inhibited cisplatin-resistant tumor growth and improved tumor-bearing mice's survival rates, indicating that FpSA switched fatty acid metabolism to glycolysis to sensitize cisplatin-resistant cells further. Taken together, cancer cell calcification induced by FpSA provides a reprogramming metabolic strategy for the treatment of chemotherapy-resistant tumors.
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| http://dx.doi.org/10.1016/j.biomaterials.2024.122886 | DOI Listing |
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