Abstract
Abstract This lack of understanding especially impacts the design of anticancer treatments. It is a common observation in the clinic that recurrent cancers, and particularly anticancer drug-resistant cancers, are more difficult to treat because they spread faster than the original tumor. CCAAT/enhancer binding protein delta (CEBPD) was activated in M2 macrophages and myofibroblasts/cancer-associated fibroblasts (CAFs) and contributed to metastasis, invasion and recurrence of cancer cells in response to PGE2 and the anticancer drugs. We further found that pentraxin 3 (PTX3) was activated in response to CEBPD induction and involved in migration and invasion of breast cancer cells, and the same phenomenon was also observed in drug-resistant cancers. Interestingly, we found that a recombinant PTX3 protein containing the C-terminal region (pPTX3) showed an opposite tumorigenic effect to the mammalian PTX3. The results suggest that PTX3 could be a promising target for preventing the metastasis/invasion of cancers and treating drug-resistant cancers. Citation Format: Jhih-Ying Chi, Ju-Ming Wang. Pentraxin 3 is responsive to the activation of CCAAT/enhancer binding delta and promotes cancer progression in the tumor microenvironment. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 926.
Published Version
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