Article Synopsis
- Tumors are adept at acquiring and using nutrients, prompting researchers to explore a method called adipose manipulation transplantation (AMT) to slow cancer progression.
- Engineered adipocytes, modified to increase glucose and fatty acid uptake, were shown to significantly suppress cancer cell growth when placed alongside tumors in various experiments.
- By transplanting these modified adipose organoids into mouse models of pancreatic and breast cancer, researchers demonstrated reduced tumor growth and vascularization, highlighting the customizable potential of AMT in targeting different cancer types.
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Article Abstract
Tumors exhibit an increased ability to obtain and metabolize nutrients. Here, we implant engineered adipocytes that outcompete tumors for nutrients and show that they can substantially reduce cancer progression, a technology termed adipose manipulation transplantation (AMT). Adipocytes engineered to use increased amounts of glucose and fatty acids by upregulating UCP1 were placed alongside cancer cells or xenografts, leading to significant cancer suppression. Transplanting modulated adipose organoids in pancreatic or breast cancer genetic mouse models suppressed their growth and decreased angiogenesis and hypoxia. Co-culturing patient-derived engineered adipocytes with tumor organoids from dissected human breast cancers significantly suppressed cancer progression and proliferation. In addition, cancer growth was impaired by inducing engineered adipose organoids to outcompete tumors using tetracycline or placing them in an integrated cell-scaffold delivery platform and implanting them next to the tumor. Finally, we show that upregulating UPP1 in adipose organoids can outcompete a uridine-dependent pancreatic ductal adenocarcinoma for uridine and suppress its growth, demonstrating the potential customization of AMT.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12319119 | PMC |
| http://dx.doi.org/10.1038/s41587-024-02551-2 | DOI Listing |
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