Journal
SCIENTIFIC REPORTS
Volume 7, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-017-06438-y
Keywords
-
Categories
Funding
- Basic Science and Platform Technology Program for Innovative Biological Medicine from Japan Agency for Medical Research and Development (AMED) [15am0301008h0002]
- Project for Cancer Research And Therapeutic Evolution (P-CREATE) from AMED [16cm0106202h0001]
- Center of Innovation (COI) program from Japan Science and Technology Agency (JST)
- JSPS KAKENHI from the Japan Society for the Promotion of Science (JSPS) [16J10727]
- JSPS [15K16331, 15H04635, 16K15104]
- Takeda Science Foundation
- Grants-in-Aid for Scientific Research [16K15104, 16K15615, 16J10727, 17H04282, 15H04635, 16F16058, 16F16407, 15K16331, 17K19698] Funding Source: KAKEN
Ask authors/readers for more resources
Increased glutamine uptake toward the elevated glutaminolysis is one of the hallmarks of tumour cells. This aberrant glutamine metabolism has recently attracted considerable attention as a diagnostic and therapeutic target. Herein, we developed glutamine-functionalized polymer to achieve a selective high affinity to tumour cells overexpressing glutaminolysis-related transporter ASCT2. In in vitro study, our developed polymer exhibited faster and higher cellular uptake in tumour cells than that in normal cells. Uptake inhibition study revealed the dominant contribution of ASCT2 to the polymer-cell interaction. Furthermore, the binding affinity of the polymer to tumour cells was estimated to be comparable to that of the potent ligand molecules reported in the literature. In in vivo study, the polymer showed prolonged retention at tumour site after intratumoral injection. This study offers a novel approach for designing tumour cell-binding synthetic polymers through the recognition of dense transporters related to tumour-associated metabolism.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available