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Host Knockout of E-prostanoid 2 receptors reduces tumor growth and causes major alterations of gene expression in prostaglandin E2-producing tumors.

Journal article
Authors Annika Gustafsson Asting
Britt-Marie Iresjö
Camilla Nilsberth
Ulrika Smedh
Kent Lundholm
Published in Oncology Letters
Volume 13
Issue 1
Pages 476-482
ISSN 1792-1074
Publication year 2017
Published at Institute of Clinical Sciences, Department of Surgery
Pages 476-482
Language en
Subject categories Cancer and Oncology


Prostaglandin E2 (PGE2) is elevated in a variety of malignant tumors and has been shown to affect several hallmarks of cancer. Accordingly, the PGE2 receptor, E‑prostanoid 2 (EP2), has been reported to be associated with patient survival and reduced tumor growth in EP2‑knockout mice. Thus, the aim of the present study was to screen for major gene expression alterations in tumor tissue growing in EP2‑knockout mice. EP2‑knockout mice were bred and implanted with EP2 receptor‑expressing and PGE2‑producing epithelial‑like tumors. Tumor tissue and plasma were collected and used for analyses with gene expression microarrays and multiplex enzyme‑linked immunosorbent assays. Tumor growth, acute phase reactions/systemic inflammation and the expression of interleukin‑6 were reduced in EP2‑knockout tumor‑bearing mice. Several hundreds of genes displayed major changes of expression in the tumor tissue when grown in EP2‑knockout mice. Such gene alterations involved several different cellular functions, including stemness, migration and cell signaling. Besides gene expression, several long non‑coding RNAs were downregulated in the tumors from the EP2‑knockout mice. Overall, PGE2 signaling via host EP2 receptors affected a large number of different genes involved in tumor progression based on signaling between host stroma and tumor cells, which caused reduced tumor growth.

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