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Molecular mechanism of [email protected] 82(OH) 22 increasing collagen expression: Implication for encaging tumor

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Gadolinium-containing fullerenol [email protected](OH)22#nbsp;has demonstrated low-toxicity and highly therapeutic efficacy in inhibiting tumor growth and metastasis through new strategy of encaging cancer, however, little is known about the mechanisms how this nanoparticle regulates fibroblast cells to prison (instead of poison) cancer cells. Here, we report that [email protected](OH)22#nbsp;promote the binding activity of tumor necrosis factor (TNFα) to tumor necrosis factor receptors 2 (TNFR2), activate TNFR2/p38 MAPK signaling pathway to increase cellular collagen expression in fibrosarcoma cells and human primary lung cancer associated fibroblasts isolated from patients. We also employ molecular dynamics simulations to study the atomic-scale mechanisms that dictate how [email protected](OH)22#nbsp;mediates interactions between TNFα and TNFRs. Our data suggest that [email protected](OH)22#nbsp;might enhance the association between TNFα and TNFR2 through a “bridge-like” mode of interaction; by contrast, the fullerenol appears to inhibit TNFα-TNFR1 association by binding to two of the receptor’s cysteine-rich domains. In concert, our results uncover a sequential, systemic process by which [email protected](OH)22#nbsp;acts to prison tumor cells, providing new insights into principles of designs of cancer therapeutics.

https://pubmed.ncbi.nlm.nih.gov/29080421/

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