Disruption of CCR1-mediated myeloid cell accumulation suppresses colorectal cancer progression in mice.


Journal

Cancer letters
ISSN: 1872-7980
Titre abrégé: Cancer Lett
Pays: Ireland
ID NLM: 7600053

Informations de publication

Date de publication:
01 09 2020
Historique:
received: 27 03 2020
revised: 12 05 2020
accepted: 20 05 2020
pubmed: 31 5 2020
medline: 13 1 2021
entrez: 31 5 2020
Statut: ppublish

Résumé

Tumor-stromal interaction is implicated in tumor progression. Although CCR1 expression in myeloid cells could be associated with pro-tumor activity, it remains elusive whether disruption of CCR1-mediated myeloid cell accumulation can suppress tumor progression. Here, we investigated the role of CCR1 depletion in myeloid cells in two syngeneic colorectal cancer mouse models: MC38, a transplanted tumor model and CMT93, a liver metastasis model. Both cells induced tumor accumulation of CCR1

Identifiants

pubmed: 32473241
pii: S0304-3835(20)30290-1
doi: 10.1016/j.canlet.2020.05.028
pii:
doi:

Substances chimiques

Vascular Endothelial Growth Factor A 0
Nitric Oxide Synthase Type II EC 1.14.13.39
SNF1-related protein kinases EC 2.7.1.-
Protein Serine-Threonine Kinases EC 2.7.11.1
Matrix Metalloproteinase 2 EC 3.4.24.24
Matrix Metalloproteinase 9 EC 3.4.24.35

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

53-62

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest MK is an employee of Kyowa Kirin Co., Ltd. All other authors declare that they have no potential conflicts of interest.

Auteurs

Yoshiyuki Kiyasu (Y)

Departments of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, 606-8507, Japan.

Kenji Kawada (K)

Departments of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, 606-8507, Japan. Electronic address: kkawada@kuhp.kyoto-u.ac.jp.

Hideyo Hirai (H)

Clinical Laboratory Medicine, Graduate School of Medicine, Kyoto University, Kyoto, 606-8507, Japan.

Ryotaro Ogawa (R)

Departments of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, 606-8507, Japan.

Keita Hanada (K)

Departments of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, 606-8507, Japan.

Hideyuki Masui (H)

Departments of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, 606-8507, Japan.

Gen Nishikawa (G)

Departments of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, 606-8507, Japan.

Takamasa Yamamoto (T)

Departments of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, 606-8507, Japan.

Rei Mizuno (R)

Departments of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, 606-8507, Japan.

Yoshiro Itatani (Y)

Departments of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, 606-8507, Japan.

Masayuki Kai (M)

Oncology Research Laboratories, Oncology R&D Unit, R&D Division, Kyowa Kirin Co., Ltd., 3-6-6 Asahi-machi, Machida, Tokyo, 194-8533, Japan.

Makoto Mark Taketo (MM)

Division of Experimental Therapeutics, Graduate School of Medicine, Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto, 606-8501, Japan.

Yoshiharu Sakai (Y)

Departments of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, 606-8507, Japan.

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Classifications MeSH