Published online Apr 14, 2016. doi: 10.3748/wjg.v22.i14.3758
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
Processing time: 213 Days and 17.1 Hours
AIM: To investigate the biological effects of internal irradiation, and the therapeutic effectiveness was assessed of 131I-labeled anti-epidermal growth factor receptor (EGFR) liposomes, derived from cetuximab, when used as a tumor-targeting carrier in a colorectal cancer mouse model.
METHODS: We described the liposomes and characterized their EGFR-targeted binding and cellular uptake in EGFR-overexpressing LS180 colorectal cancer cells. After intra-tumor injections of 74 MBq (740 MBq/mL) 131I-antiEGFR-BSA-PCL, we investigated the biological effects of internal irradiation and the therapeutic efficacy of 131I-antiEGFR-BSA-PCL on colorectal cancer in a male BALB/c mouse model. Tumor size, body weight, histopathology, and SPECT imaging were monitored for 33 d post-therapy.
RESULTS: The rapid radioiodine uptake of 131I-antiEGFR-BSA-PCL and 131I-BSA-PCL reached maximum levels at 4 h after incubation, and the 131I uptake of 131I-antiEGFR-BSA-PCL was higher than that of 131I-BSA-PCL in vitro. The 131I tissue distribution assay revealed that 131I-antiEGFR-BSA-PCL was markedly taken up by the tumor. Furthermore, a tissue distribution assay revealed that 131I-antiEGFR-BSA-PCL was markedly taken up by the tumor and reached its maximal uptake value of 21.0 ± 1.01 %ID/g (%ID/g is the percentage injected dose per gram of tissue) at 72 h following therapy; the drug concentration in the tumor was higher than that in the liver, heart, colon, or spleen. Tumor size measurements showed that tumor development was significantly inhibited by treatments with 131I-antiEGFR-BSA-PCL and 131I-BSA-PCL. The volume of tumor increased, and treatment rate with 131I-antiEGFR-BSA-PCL was 124% ± 7%, lower than that with 131I-BSA-PCL (127% ± 9%), 131I (143% ± 7%), and normal saline (146% ± 10%). The percentage losses in original body weights were 39% ± 3%, 41% ± 4%, 49% ± 5%, and 55% ± 13%, respectively. The best survival and cure rates were obtained in the group treated with 131I-antiEGFR-BSA-PCL. The animals injected with 131I-antiEGFR-BSA-PCL and 131I-BSA-PCL showed more uniform focused liposome distribution within the tumor area.
CONCLUSION: This study demonstrated the potential beneficial application of 131I-antiEGFR-BSA-PCL for treating colorectal cancer. 131I-antiEGFR-BSA-PCL suppressed the development of xenografted colorectal cancer in nude mice, thereby providing a novel candidate for receptor-mediated targeted radiotherapy.
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.