α‐Emitting cancer therapy using (211)At‐AAMT targeting LAT1

α‐Methyl‐l‐tyrosine (AMT) has a high affinity for the cancer‐specific l‐type amino acid transporter 1 (LAT1). Therefore, we established an anti‐cancer therapy, with (211)At‐labeled α‐methyl‐l‐tyrosine ((211)At‐AAMT) as a carrier of (211)At into tumors. (211)At‐AAMT had high affinity for LAT1, inhibi...

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Autores principales: Kaneda‐Nakashima, Kazuko, Zhang, ZiJian, Manabe, Yoshiyuki, Shimoyama, Atsushi, Kabayama, Kazuya, Watabe, Tadashi, Kanai, Yoshikatsu, Ooe, Kazuhiro, Toyoshima, Atsushi, Shirakami, Yoshifumi, Yoshimura, Takashi, Fukuda, Mitsuhiro, Hatazawa, Jun, Nakano, Takashi, Fukase, Koichi, Shinohara, Atsushi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Original Articles
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7935802/
https://www.ncbi.nlm.nih.gov/pubmed/33277750
http://dx.doi.org/10.1111/cas.14761
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author Kaneda‐Nakashima, Kazuko
Zhang, ZiJian
Manabe, Yoshiyuki
Shimoyama, Atsushi
Kabayama, Kazuya
Watabe, Tadashi
Kanai, Yoshikatsu
Ooe, Kazuhiro
Toyoshima, Atsushi
Shirakami, Yoshifumi
Yoshimura, Takashi
Fukuda, Mitsuhiro
Hatazawa, Jun
Nakano, Takashi
Fukase, Koichi
Shinohara, Atsushi
author_facet Kaneda‐Nakashima, Kazuko
Zhang, ZiJian
Manabe, Yoshiyuki
Shimoyama, Atsushi
Kabayama, Kazuya
Watabe, Tadashi
Kanai, Yoshikatsu
Ooe, Kazuhiro
Toyoshima, Atsushi
Shirakami, Yoshifumi
Yoshimura, Takashi
Fukuda, Mitsuhiro
Hatazawa, Jun
Nakano, Takashi
Fukase, Koichi
Shinohara, Atsushi
author_sort Kaneda‐Nakashima, Kazuko
collection PubMed
description α‐Methyl‐l‐tyrosine (AMT) has a high affinity for the cancer‐specific l‐type amino acid transporter 1 (LAT1). Therefore, we established an anti‐cancer therapy, with (211)At‐labeled α‐methyl‐l‐tyrosine ((211)At‐AAMT) as a carrier of (211)At into tumors. (211)At‐AAMT had high affinity for LAT1, inhibited tumor cell growth, and induced DNA double‐stranded breaks in vitro. We evaluated the accumulation of (211)At‐AAMT in vivo and the role of LAT1. Treatment with 0.4 MBq/mouse (211)At‐AAMT inhibited tumor growth in the PANC‐1 tumor model and 1 MBq/mouse (211)At‐AAMT inhibited metastasis in the lung of the B16F10 metastasis model. Our results suggested that (211)At would be useful for anti‐cancer therapy and that LAT1 is suitable as a target for radionuclide therapy.
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spelling pubmed-79358022021-03-15 α‐Emitting cancer therapy using (211)At‐AAMT targeting LAT1 Kaneda‐Nakashima, Kazuko Zhang, ZiJian Manabe, Yoshiyuki Shimoyama, Atsushi Kabayama, Kazuya Watabe, Tadashi Kanai, Yoshikatsu Ooe, Kazuhiro Toyoshima, Atsushi Shirakami, Yoshifumi Yoshimura, Takashi Fukuda, Mitsuhiro Hatazawa, Jun Nakano, Takashi Fukase, Koichi Shinohara, Atsushi Cancer Sci Original Articles α‐Methyl‐l‐tyrosine (AMT) has a high affinity for the cancer‐specific l‐type amino acid transporter 1 (LAT1). Therefore, we established an anti‐cancer therapy, with (211)At‐labeled α‐methyl‐l‐tyrosine ((211)At‐AAMT) as a carrier of (211)At into tumors. (211)At‐AAMT had high affinity for LAT1, inhibited tumor cell growth, and induced DNA double‐stranded breaks in vitro. We evaluated the accumulation of (211)At‐AAMT in vivo and the role of LAT1. Treatment with 0.4 MBq/mouse (211)At‐AAMT inhibited tumor growth in the PANC‐1 tumor model and 1 MBq/mouse (211)At‐AAMT inhibited metastasis in the lung of the B16F10 metastasis model. Our results suggested that (211)At would be useful for anti‐cancer therapy and that LAT1 is suitable as a target for radionuclide therapy. John Wiley and Sons Inc. 2021-01-22 2021-03 /pmc/articles/PMC7935802/ /pubmed/33277750 http://dx.doi.org/10.1111/cas.14761 Text en © 2020 The Authors. Cancer Science published by John Wiley & Sons Australia, Ltd on behalf of Japanese Cancer Association. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Original Articles
Kaneda‐Nakashima, Kazuko
Zhang, ZiJian
Manabe, Yoshiyuki
Shimoyama, Atsushi
Kabayama, Kazuya
Watabe, Tadashi
Kanai, Yoshikatsu
Ooe, Kazuhiro
Toyoshima, Atsushi
Shirakami, Yoshifumi
Yoshimura, Takashi
Fukuda, Mitsuhiro
Hatazawa, Jun
Nakano, Takashi
Fukase, Koichi
Shinohara, Atsushi
α‐Emitting cancer therapy using (211)At‐AAMT targeting LAT1
title α‐Emitting cancer therapy using (211)At‐AAMT targeting LAT1
title_full α‐Emitting cancer therapy using (211)At‐AAMT targeting LAT1
title_fullStr α‐Emitting cancer therapy using (211)At‐AAMT targeting LAT1
title_full_unstemmed α‐Emitting cancer therapy using (211)At‐AAMT targeting LAT1
title_short α‐Emitting cancer therapy using (211)At‐AAMT targeting LAT1
title_sort α‐emitting cancer therapy using (211)at‐aamt targeting lat1
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7935802/
https://www.ncbi.nlm.nih.gov/pubmed/33277750
http://dx.doi.org/10.1111/cas.14761
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