Next Article in Journal
Molecular Pathways Involved in the Amelioration of Myocardial Injury in Diabetic Rats by Kaempferol
Next Article in Special Issue
p53 Expression as a Diagnostic Biomarker in Ulcerative Colitis-Associated Cancer
Previous Article in Journal
Human Chorionic Gonadotropin: The Pregnancy Hormone and More
Previous Article in Special Issue
Role of the Vanins–Myeloperoxidase Axis in Colorectal Carcinogenesis
Article Menu
Issue 5 (May) cover image

Export Article

Open AccessArticle
Int. J. Mol. Sci. 2017, 18(5), 1058; doi:10.3390/ijms18051058

Osteopontin Deficiency Suppresses Intestinal Tumor Development in Apc-Deficient Min Mice

1
Central Animal Division, National Cancer Center Research Institute, 5-1-1, Tsukiji, Chuo-ku, Tokyo 104-0045, Japan
2
Epidemiology and Prevention Division, Research Center for Cancer Prevention and Screening, National Cancer Center, 5-1-1, Tsukiji, Chuo-ku, Tokyo 104-0045, Japan
3
Division of Pathology, National Institute of Health Science, 1-18-1 Kamiyoga, Setagaya-ku, Tokyo 158-8501, Japan
*
Author to whom correspondence should be addressed.
Academic Editors: Takuji Tanaka and Masahito Shimizu
Received: 29 March 2017 / Revised: 5 May 2017 / Accepted: 9 May 2017 / Published: 14 May 2017
(This article belongs to the Special Issue Inflammation and Cancer)
View Full-Text   |   Download PDF [3036 KB, uploaded 14 May 2017]   |  

Abstract

Osteopontin (OPN) is a secreted phosphoglycoprotein, and is a transcriptional target of aberrant Wnt signaling. OPN is upregulated in human colon cancers, and is suggested to enhance cancer progression. In this study, the effect of deficiency of OPN on intestinal tumor development in Apc-deficient Min mice was investigated. At 16 weeks of age, the number of small intestinal polyps in Min/OPN(+/−) and Min/OPN(−/−) mice was lower than that of Min/OPN(+/+) mice. Colorectal tumor incidences and multiplicities in Min/OPN(+/−) and Min/OPN(−/−) mice were significantly lower than those in Min/OPN(+/+) mice, being 48% and 0.6 ± 0.8, 50% and 0.8 ± 0.9 vs. 80% and 1.6 ± 1.7, respectively. OPN expression in colorectal tumors was strongly upregulated in Min/OPN(+/+) compared to adjacent non-tumor parts, but was decreased in Min/OPN(+/−) and not detected in Min/OPN(−/−). Targets of OPN, matrix metalloproteinases (MMPs)-3, -9, and -13 were lowered by OPN deficiency. Macrophage marker F4/80 in colorectal tumors was also lowered by OPN deficiency. MMP-9 expression was observed in tumor cells and tumor-infiltrating neutrophils. These results indicate that induction of OPN by aberrant Wnt signaling could enhance colorectal tumor development in part by upregulation of MMP-3, -9, and -13 and infiltration of macrophage and neutrophils. Suppression of OPN expression could contribute to tumor prevention, but complete deficiency of OPN may cause some adverse effects. View Full-Text
Keywords: osteopontin; colorectal tumor; macrophage osteopontin; colorectal tumor; macrophage
Figures

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Supplementary material

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Ishigamori, R.; Komiya, M.; Takasu, S.; Mutoh, M.; Imai, T.; Takahashi, M. Osteopontin Deficiency Suppresses Intestinal Tumor Development in Apc-Deficient Min Mice. Int. J. Mol. Sci. 2017, 18, 1058.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top