Loss of SMAD4 Promotes Colorectal Cancer Progression by Recruiting Tumor-Associated Neutrophils via the CXCL1/8-CXCR2 Axis.


Journal

Clinical cancer research : an official journal of the American Association for Cancer Research
ISSN: 1557-3265
Titre abrégé: Clin Cancer Res
Pays: United States
ID NLM: 9502500

Informations de publication

Date de publication:
01 05 2019
Historique:
received: 09 11 2018
revised: 04 01 2019
accepted: 28 01 2019
pubmed: 2 2 2019
medline: 20 6 2020
entrez: 2 2 2019
Statut: ppublish

Résumé

SMAD4 is a key transcriptional factor of TGFβ signaling and acts as a tumor suppressor in colorectal cancer. In the present study, we explored the immunologic effect of SMAD4 on the tumor microenvironment. Using 99 clinical specimens and human colorectal cancer cell lines, we investigate the relationship between SMAD4 expression and neutrophil accumulation. We immunohistochemically analyzed expression of SMAD4, CXCL1, CXCL8, CXCR2, and other proteins with clinical specimens. Finally, we determined the serum levels of CXCL1 and CXCL8 in 125 patients with colorectal cancer. SMAD4 knockdown from human colorectal cancer cells upregulated the expression of CXCL1 and CXCL8, which recruited neutrophils to colorectal cancer tumor via CXCR2. In turn, when neutrophils were exposed to the supernatant of SMAD4-negative colorectal cancer cells, they produced a large amount of CXCL1 and CXCL8 by themselves Blockade of the CXCL1/8-CXCR2 axis could be a novel therapeutic approach against SMAD4-negative colorectal cancer.

Identifiants

pubmed: 30705034
pii: 1078-0432.CCR-18-3684
doi: 10.1158/1078-0432.CCR-18-3684
doi:

Substances chimiques

Biomarkers, Tumor 0
CXCL1 protein, human 0
CXCL8 protein, human 0
CXCR2 protein, human 0
Chemokine CXCL1 0
Interleukin-8 0
Receptors, Interleukin-8B 0
SMAD4 protein, human 0
Smad4 Protein 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

2887-2899

Informations de copyright

©2019 American Association for Cancer Research.

Auteurs

Ryotaro Ogawa (R)

Department of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Takamasa Yamamoto (T)

Department of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Hideyo Hirai (H)

Department of Transfusion Medicine and Cell Therapy, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Keita Hanada (K)

Department of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Yoshiyuki Kiyasu (Y)

Department of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Gen Nishikawa (G)

Department of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Rei Mizuno (R)

Department of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Susumu Inamoto (S)

Department of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Yoshiro Itatani (Y)

Department of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Yoshiharu Sakai (Y)

Department of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Kenji Kawada (K)

Department of Surgery, Graduate School of Medicine, Kyoto University, Kyoto, Japan. kkawada@kuhp.kyoto-u.ac.jp.

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Classifications MeSH