Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/116032
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Type: Journal article
Title: CXCR4-expressing Mist1+ progenitors in the gastric antrum contribute to gastric cancer development
Author: Sakitani, K.
Hayakawa, Y.
Deng, H.
Ariyama, H.
Kinoshita, H.
Konishi, M.
Ono, S.
Suzuki, N.
Ihara, S.
Niu, Z.
Kim, W.
Tanaka, T.
Liu, H.
Chen, X.
Tailor, Y.
Fox, J.
Konieczny, S.
Onodera, H.
Sepulveda, A.
Asfaha, S.
et al.
Citation: Oncotarget, 2017; 8(67):111012-111025
Publisher: Impact Journals
Issue Date: 2017
ISSN: 1949-2553
1949-2553
Statement of
Responsibility: 
Kosuke Sakitani, Yoku Hayakawa, Huan Deng, Hiroshi Ariyama, Hiroto Kinoshita ... Daniel L. Worthley... et al.
Abstract: Mist1 was recently shown to identify a discrete population of stem cells within the isthmus of the oxyntic gland within the gastric corpus. Chief cells at the base of the gastric corpus also express Mist1. The relevance of Mist1 expression as a marker of specific cell populations within the antral glands of the distal stomach, however, is unknown. Using Mist1-CreERT mice, we revealed that Mist1+ antral cells, distinct from the Mist1+ population in the corpus, comprise long-lived progenitors that reside within the antral isthmus above Lgr5+ or CCK2R+ cells. Mist1+ antral progenitors can serve as an origin of antral tumors induced by loss of Apc or MNU treatment. Mist1+ antral progenitors, as well as other antral stem/progenitor population, express Cxcr4, and are located in close proximity to Cxcl12 (the Cxcr4 ligand)-expressing endothelium. During antral carcinogenesis, there is an expansion of Cxcr4+ epithelial cells as well as the Cxcl12+ perivascular niche. Deletion of Cxcl12 in endothelial cells or pharmacological blockade of Cxcr4 inhibits antral tumor growth. Cxcl12/Cxcr4 signaling may be a potential therapeutic target.
Keywords: cxcl12
cxcr4
gastric cancer
mist1
stem cell
Rights: Sakitani et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
DOI: 10.18632/oncotarget.22451
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