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      Immunohistochemical Demonstration of Membrane-bound Prostaglandin E 2 Synthase-1 in Papillary Thyroid Carcinoma

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          Abstract

          Microsomal prostaglandin E 2 synthase-1 (mPGES-1) is an inducible enzyme that catalyzes the conversion of prostaglandin (PG) H 2 to PGE 2 in downstream of cyclooxygenase-2 (COX-2). Recent studies have obtained in vitro evidence that PGE 2 participates in carcinogenesis, angiogenesis, and induction of matrix metalloproteinase-9 (MMP-9), which plays a crucial role in cancer invasion. However, implications for mPGES-1 in thyroid carcinomas remain to be determined. To address this issue, we performed an immunohistochemical analysis for mPGES-1, COX-2 and MMP-9 in 20 papillary thyroid carcinoma (PTC) patients. mPGES-1 immunoreactivity was localized in the cytoplasm of carcinoma cells in 19 cases, with an intensity that tended to be distinct at the interface between the tumor and the surrounding non-neoplastic tissue. Staining was more intense in regions with papillary arrangement, while it was less intense in regions with trabecular or solid arrangement. In many cases, immunohistochemical localization of COX-2 and MMP-9 resemble that of mPGES-1. Taken together, our results suggest the involvement of mPGES-1 in proliferation and differentiation of PTC as well as local invasion of PTC.

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          Acceleration of intestinal polyposis through prostaglandin receptor EP2 in Apc(Delta 716) knockout mice.

          Shuh Narumiya, M Sonoshita, K Takaku … (2001)
          Arachidonic acid is metabolized to prostaglandin H(2) (PGH(2)) by cyclooxygenase (COX). COX-2, the inducible COX isozyme, has a key role in intestinal polyposis. Among the metabolites of PGH(2), PGE(2) is implicated in tumorigenesis because its level is markedly elevated in tissues of intestinal adenoma and colon cancer. Here we show that homozygous deletion of the gene encoding a cell-surface receptor of PGE(2), EP2, causes decreases in number and size of intestinal polyps in Apc(Delta 716) mice (a mouse model for human familial adenomatous polyposis). This effect is similar to that of COX-2 gene disruption. We also show that COX-2 expression is boosted by PGE(2) through the EP2 receptor via a positive feedback loop. Homozygous gene knockout for other PGE(2) receptors, EP1 or EP3, did not affect intestinal polyp formation in Apc(Delta 716) mice. We conclude that EP2 is the major receptor mediating the PGE2 signal generated by COX-2 upregulation in intestinal polyposis, and that increased cellular cAMP stimulates expression of more COX-2 and vascular endothelial growth factor in the polyp stroma.
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            Prostaglandin E(2) promotes colorectal adenoma growth via transactivation of the nuclear peroxisome proliferator-activated receptor delta.

            Qiong Shi, Beatrice Desvergne, Dingzhi Wang … (2004)
            Cyclooxygenase-derived prostaglandin E(2) (PGE(2)) is the predominant prostanoid found in most colorectal cancers (CRC) and is known to promote colon carcinoma growth and invasion. However, the key downstream signaling pathways necessary for PGE(2)-induced intestinal carcinogenesis are unclear. Here we report that PGE(2) indirectly transactivates PPARdelta through PI3K/Akt signaling, which promotes cell survival and intestinal adenoma formation. We also found that PGE(2) treatment of Apc(min) mice dramatically increased intestinal adenoma burden, which was negated in Apc(min) mice lacking PPARdelta. We demonstrate that PPARdelta is a focal point of crosstalk between the prostaglandin and Wnt signaling pathways which results in a shift from cell death to cell survival, leading to increased tumor growth.
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              RET/PTC rearrangement in thyroid tumors.

              Yuri E. Nikiforov (2001)
              Rearrangement of the RET gene, also known as RET/PTC rearrangement, is the most common genetic alteration identified to date in thyroid papillary carcinomas. The prevalence of RET/PTC in papillary carcinomas shows significant geographic variation and is approx 35% in North America. RET/PTC is more common in tumors in children and young adults, and in papillary carcinomas associated with radiation exposure. There are at least 10 different types of RET/PTC, all resulting from the fusion of the tyrosine kinase domain of RET to the 5' portion of different genes. RET/PTC1 and RET/PTC3 are the most common types, accounting for >90% of all rearrangements. There is some evidence that different types of RET/PTC may be associated with distinct biologic properties of papillary carcinomas. RET/PTC1 tends to be more common in tumors with typical papillary growth and microcarcinomas and to have a more benign clinical course, whereas RET/PTC3 in some populations shows a strong correlation with the solid variant of papillary carcinoma and more aggressive tumor behavior. RET/PTC has recently been found in hyalinizing trabecular adenomas of the thyroid gland, providing molecular evidence in favor of this tumor to be a variant of papillary carcinoma. The occurrence of RET/PTC in Hashimoto thyroiditis and thyroid follicular adenomas and hyperplastic nodules reported in several studies has not been confirmed in other observations and remains controversial.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Acta Histochem Cytochem
                Journal ID (publisher-id): AHC
                Title: Acta Histochemica et Cytochemica
                Publisher: Japan Society of Histochemistry and Cytochemistry (Tokyo, Japan )
                ISSN (Print): 0044-5991
                ISSN (Electronic): 1347-5800
                Publication date (Print): 29 August 2009
                Publication date (Electronic): 14 July 2009
                Volume: 42
                Issue: 4
                Pages: 105-109
                Affiliations
                [1 ]Department of Pathology, Tokyo Women’s Medical University
                [2 ]Department of Endocrine Surgery, Tokyo Women’s Medical University, 8–1 Kawada-cho, Shinjuku-ku, Tokyo 162–8666, Japan
                Author notes
                Correspondence to: Yoko Omi, M.D., Department of Pathology, Graduate School of Medicine, Tokyo Women’s Medical University, 8–1 Kawada-cho, Shinjuku-ku, Tokyo 162–8666, Japan. E-mail: yomi@ 123456research.twmu.ac.jp
                Article
                Publisher ID: AHC09014
                DOI: 10.1267/ahc.09014
                PMC ID: 2742720
                PubMed ID: 19759871
                SO-VID: 8fc07711-4aa5-40ab-9242-d708116bf227
                Copyright © © 2009 The Japan Society of Histochemistry and Cytochemistry
                License:

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

                History
                Date received : 26 March 2009
                Date accepted : 14 May 2009
                Categories
                Subject: Regular Article

                ScienceOpen disciplines: Clinical chemistry
                Keywords: papillary thyroid carcinoma,cyclooxygenase-2,prostaglandin e synthase,matrix metalloproteinase,immunohistochemistry
                Data availability:
                ScienceOpen disciplines: Clinical chemistry
                Keywords: papillary thyroid carcinoma, cyclooxygenase-2, prostaglandin e synthase, matrix metalloproteinase, immunohistochemistry

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