Reply to Comment on “Kadomoto, S. et al. Tumor-Associated Macrophages Induce Migration of Renal Cell Carcinoma Cells via Activation of the CCL20-CCR6 Axis” Cancers 2020 12, 89
We appreciate Zins and Abraham [1] commenting on our paper studying the role of the CCL20-CCR6 axis on renal cell carcinoma (RCC) cells [2]. As they pointed out, our study has certain limitations. Although M1- and M2-types cannot be separated clearly and a consecutive change of character might exist...
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doaj-05d278cfec8841b286513ab8d2cc3b232020-11-25T01:30:14ZengMDPI AGCancers2072-66942020-02-0112235410.3390/cancers12020354cancers12020354Reply to Comment on “Kadomoto, S. et al. Tumor-Associated Macrophages Induce Migration of Renal Cell Carcinoma Cells via Activation of the CCL20-CCR6 Axis” Cancers 2020 12, 89Suguru Kadomoto0Kouji Izumi1Kaoru Hiratsuka2Taito Nakano3Renato Naito4Tomoyuki Makino5Hiroaki Iwamoto6Hiroshi Yaegashi7Kazuyoshi Shigehara8Yoshifumi Kadono9Hiroki Nakata10Yohei Saito11Kyoko Nakagawa-Goto12Atsushi Mizokami13Department of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa 920-8641, JapanDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa 920-8641, JapanDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa 920-8641, JapanDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa 920-8641, JapanDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa 920-8641, JapanDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa 920-8641, JapanDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa 920-8641, JapanDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa 920-8641, JapanDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa 920-8641, JapanDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa 920-8641, JapanDepartment of Histology and Cell Biology, Kanazawa University Graduate School of Medical Science, Kanazawa 920-8641, JapanSchool of Pharmaceutical Sciences, College of Medical, Pharmaceutical and Health Science, Kanazawa University, Kanazawa 920-1192, JapanSchool of Pharmaceutical Sciences, College of Medical, Pharmaceutical and Health Science, Kanazawa University, Kanazawa 920-1192, JapanDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa 920-8641, JapanWe appreciate Zins and Abraham [1] commenting on our paper studying the role of the CCL20-CCR6 axis on renal cell carcinoma (RCC) cells [2]. As they pointed out, our study has certain limitations. Although M1- and M2-types cannot be separated clearly and a consecutive change of character might exist between them, it has been reported that plural specific markers express on M1- and M2-types. Unfortunately, a definite difference between M1 and M2 macrophages was not confirmed in our study. For more differentiation, multiple stimulations, such as suggested in the comments of Zins and Abraham, might be needed. Hence, we needed to expediently use “M1-like” and “M2-like” to mention specific status of these macrophage-like cells. Meanwhile, CCL20 expression levels of M2-like-THP-1 cells co-cultured with RCC cells were dramatically increased compared with parental THP-1 cells, indicating that certain stimulations within the tumor microenvironment rather than theoretical stimulations make macrophages differentiated; however, further studies are needed to clarify this mechanism using a more appropriate co-culture system mimicking the tumor microenvironment. Immunohistochemistry of CCL20 and M2 markers will help to better understand the role of tissue infiltrating macrophages, even tissue CD68 staining intensity itself was reported to correlate with prognosis of RCC patients [3]. [...]https://www.mdpi.com/2072-6694/12/2/354n/a |
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English |
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Article |
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DOAJ |
author |
Suguru Kadomoto Kouji Izumi Kaoru Hiratsuka Taito Nakano Renato Naito Tomoyuki Makino Hiroaki Iwamoto Hiroshi Yaegashi Kazuyoshi Shigehara Yoshifumi Kadono Hiroki Nakata Yohei Saito Kyoko Nakagawa-Goto Atsushi Mizokami |
spellingShingle |
Suguru Kadomoto Kouji Izumi Kaoru Hiratsuka Taito Nakano Renato Naito Tomoyuki Makino Hiroaki Iwamoto Hiroshi Yaegashi Kazuyoshi Shigehara Yoshifumi Kadono Hiroki Nakata Yohei Saito Kyoko Nakagawa-Goto Atsushi Mizokami Reply to Comment on “Kadomoto, S. et al. Tumor-Associated Macrophages Induce Migration of Renal Cell Carcinoma Cells via Activation of the CCL20-CCR6 Axis” Cancers 2020 12, 89 Cancers n/a |
author_facet |
Suguru Kadomoto Kouji Izumi Kaoru Hiratsuka Taito Nakano Renato Naito Tomoyuki Makino Hiroaki Iwamoto Hiroshi Yaegashi Kazuyoshi Shigehara Yoshifumi Kadono Hiroki Nakata Yohei Saito Kyoko Nakagawa-Goto Atsushi Mizokami |
author_sort |
Suguru Kadomoto |
title |
Reply to Comment on “Kadomoto, S. et al. Tumor-Associated Macrophages Induce Migration of Renal Cell Carcinoma Cells via Activation of the CCL20-CCR6 Axis” Cancers 2020 12, 89 |
title_short |
Reply to Comment on “Kadomoto, S. et al. Tumor-Associated Macrophages Induce Migration of Renal Cell Carcinoma Cells via Activation of the CCL20-CCR6 Axis” Cancers 2020 12, 89 |
title_full |
Reply to Comment on “Kadomoto, S. et al. Tumor-Associated Macrophages Induce Migration of Renal Cell Carcinoma Cells via Activation of the CCL20-CCR6 Axis” Cancers 2020 12, 89 |
title_fullStr |
Reply to Comment on “Kadomoto, S. et al. Tumor-Associated Macrophages Induce Migration of Renal Cell Carcinoma Cells via Activation of the CCL20-CCR6 Axis” Cancers 2020 12, 89 |
title_full_unstemmed |
Reply to Comment on “Kadomoto, S. et al. Tumor-Associated Macrophages Induce Migration of Renal Cell Carcinoma Cells via Activation of the CCL20-CCR6 Axis” Cancers 2020 12, 89 |
title_sort |
reply to comment on “kadomoto, s. et al. tumor-associated macrophages induce migration of renal cell carcinoma cells via activation of the ccl20-ccr6 axis” cancers 2020 12, 89 |
publisher |
MDPI AG |
series |
Cancers |
issn |
2072-6694 |
publishDate |
2020-02-01 |
description |
We appreciate Zins and Abraham [1] commenting on our paper studying the role of the CCL20-CCR6 axis on renal cell carcinoma (RCC) cells [2]. As they pointed out, our study has certain limitations. Although M1- and M2-types cannot be separated clearly and a consecutive change of character might exist between them, it has been reported that plural specific markers express on M1- and M2-types. Unfortunately, a definite difference between M1 and M2 macrophages was not confirmed in our study. For more differentiation, multiple stimulations, such as suggested in the comments of Zins and Abraham, might be needed. Hence, we needed to expediently use “M1-like” and “M2-like” to mention specific status of these macrophage-like cells. Meanwhile, CCL20 expression levels of M2-like-THP-1 cells co-cultured with RCC cells were dramatically increased compared with parental THP-1 cells, indicating that certain stimulations within the tumor microenvironment rather than theoretical stimulations make macrophages differentiated; however, further studies are needed to clarify this mechanism using a more appropriate co-culture system mimicking the tumor microenvironment. Immunohistochemistry of CCL20 and M2 markers will help to better understand the role of tissue infiltrating macrophages, even tissue CD68 staining intensity itself was reported to correlate with prognosis of RCC patients [3]. [...] |
topic |
n/a |
url |
https://www.mdpi.com/2072-6694/12/2/354 |
work_keys_str_mv |
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