Basic Study
Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Apr 14, 2016; 22(14): 3758-3768
Published online Apr 14, 2016. doi: 10.3748/wjg.v22.i14.3758
Evaluation of therapeutic effectiveness of 131I-antiEGFR-BSA-PCL in a mouse model of colorectal cancer
Wei Li, Yan-Hui Ji, Cheng-Xia Li, Zhong-Yun Liu, Ning Li, Lei Fang, Jin Chang, Jian Tan
Wei Li, Yan-Hui Ji, Cheng-Xia Li, Ning Li, Jian Tan, Department of Nuclear Medicine, Tianjin Medical University General Hospital, Tianjin 300052, China
Zhong-Yun Liu, Yantai Institute of Coastal Zone Research, Chinese Academy of Sciences, Yantai 264003, Shandong Province, China
Lei Fang, Jin Chang, Institute of Nanobiotechnology, School of Materials Science and Engineering, Tianjin Key Laboratory of Composites and Functional Materials, Tianjin University, Tianjin 300072, China
Author contributions: Li W and Ji YH have contributed equally to this work, and they substantially contributed to the conception and design of the study and the acquisition of the data; Li CX, Liu ZY, Li N, Fang L, Chang J and Tan J analyzed and interpreted the data; Li W and Ji YH drafted the article, made critical revisions related to the intellectual content of the manuscript, and approved the final version of the article to be published.
Supported by the National Natural Science Foundation of China, No. 81301244 (to Li W); and the National Key Clinical Specialty Project.
Institutional animal care and use committee statement: This study was performed in accordance with the guidelines of the National Institutes of Health Guide for the Care and Use of Laboratory Animals and was approved by the Animal Care and Use Committee of Tianjin Medical University.
Conflict-of-interest statement: To the best of our knowledge, no conflict of interest exists.
Data sharing statement: The technical appendix, statistical code, and dataset are available from the corresponding author at (tanpost@163.com). Participants gave informed consent for data sharing. The authors confirm that all data underlying the findings are fully available without restriction. All relevant data are mentioned in the paper. No additional data are available.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Jian Tan, MD, Professor of Medicine, Chief, Department of Nuclear Medicine, Tianjin Medical University General Hospital, Anshan Road 154, Heping District, Tianjin 300052, China. tanpost@163.com
Telephone: +86-22-60362881
Received: August 28, 2015
Peer-review started: September 1, 2015
First decision: September 29, 2015
Revised: November 2, 2015
Accepted: January 17, 2016
Article in press: January 19, 2016
Published online: April 14, 2016
Core Tip

Core tip: This paper describes liposomes that were assessed for EGFR-targeted binding and cellular uptake in EGFR-overexpressing LS180 colorectal cancer cells and a mouse model of colorectal cancer. Anti-EGFR and non-targeted liposomes were labeled with 131I using the chloramine-T method. The time-dependent cellular uptake of 131I-antiEGFR-BSA-PCL and 131I-BSA-PCL demonstrated the slow-release effects of nanoparticles. The results of confocal microscopic analysis revealed the significant uptake of antiEGFR-BSA-PCL in LS180 cells. This study also investigated the biological effects of internal irradiation and the therapeutic efficacy of 131I-antiEGFR-BSA-PCL on colorectal cancer in a BALB/c mouse model. To address this issue, tumor size, body weight, histopathology, and SPECT imaging were monitored for 33 d post-therapy. The 131I-antiEGFR-BSA-PCL was demonstrated to be superior in regard to cellular binding and uptake compared with control BSA-PCL in the mouse model.