Elevated expression of endocan in the development of cervical squamous neoplasia of the uterus.

Cervical squamous intraepithelial neoplasia Endocan Immunohistochemistry Retinoic acid-metabolizing enzyme CYP26A1 Squamous cell carcinoma Uterus

Journal

Medical molecular morphology
ISSN: 1860-1499
Titre abrégé: Med Mol Morphol
Pays: Japan
ID NLM: 101239023

Informations de publication

Date de publication:
Sep 2023
Historique:
received: 11 03 2023
accepted: 09 04 2023
medline: 14 8 2023
pubmed: 19 4 2023
entrez: 19 04 2023
Statut: ppublish

Résumé

Accumulated evidence has shown that endocan, which was originally called endothelial cell-specific molecule-1, is an attractive prognostic factor in a variety of cancers. However, the relevance of endocan expression in human malignancies remains to be clarified. In the present study, the expression of endocan in cervical squamous neoplasia of the uterus, including low- and high-grade squamous intraepithelial lesions (LSIL and HSIL, respectively), as well as in invasive squamous cell carcinoma was examined by immunohistochemistry. Endocan was not sufficiently expressed in the normal cervical epithelium. Endocan expression was present in LSIL cases but was limited to basal and parabasal areas of the cells. HSIL cases exhibited strong expression of endocan with widely distributed expression toward the epithelial surface. In contrast, further strong expression of endocan was not observed in patients with invasive carcinoma. This study is the first study showing increased expression of endocan in precancerous dysplastic lesions and malignancy of the cervix. The data suggest that a high expression level of endocan potentially contributes to the development of cervical squamous neoplasia of the uterus.

Identifiants

pubmed: 37074500
doi: 10.1007/s00795-023-00353-0
pii: 10.1007/s00795-023-00353-0
doi:

Substances chimiques

ESM1 protein, human 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

187-193

Informations de copyright

© 2023. The Author(s) under exclusive licence to The Japanese Society for Clinical Molecular Morphology.

Références

Lassalle P, Molet S, Janin A, Heyden JV, Tavernier J, Fiers W, Devos R, Tonnel AB (1996) ESM-1 is a novel human endothelial cell-specific molecule expressed in lung and regulated by cytokines. J Biol Chem 271:20458–20464
doi: 10.1074/jbc.271.34.20458 pubmed: 8702785
Zhang SM, Zuo L, Zhou Q, Gui SY, Shi R, Wu Q, Wei W, Wang Y (2012) Expression and distribution of endocan in human tissues. Biotech Histochem 87:172–178
doi: 10.3109/10520295.2011.577754 pubmed: 21526908
Sarrazin S, Adam E, Lyon M, Depontieu F, Motte V, Landolfi C, Lortat-Jacob H, Bechard D, Lassalle P, Delehedde M (2006) Endocan or endothelial cell specific molecule-1 (ESM-1): a potential novel endothelial cell marker and a new target for cancer therapy. Biochim Biophys Acta 1765:25–37
pubmed: 16168566
Öztop N, Özer PK, Demir S, Beyaz S, Tiryaki TO, Özkan G, Aydogan M, Bugra MZZ, Çolakoglu B, Büyüköztürkn S, Nalçacı M, Yavuz AS, Gelincik A (2021) Impaired endothelial function irrespective of systemic inflammation or atherosclerosis in mastocytosis. Ann Allergy Asthma Immunol 127:76–82
doi: 10.1016/j.anai.2021.03.020 pubmed: 33775901
Rocha SF, Schiller M, Jing D, Li H, Butz S, Vestweber D, Biljes D, Drexler HCA, Nieminen-Kelhä M, Vajkoczy P, Adams S, Benedito R, Adams RH (2014) sm1 modulates endothelial tip cell behavior and vascular permeability by enhancing VEGF bioavailability. Circ Res 115:581–590
doi: 10.1161/CIRCRESAHA.115.304718 pubmed: 25057127
Lu J, Liu Q, Zhu L, Liu Y, Zhu X, Peng S, Chen M, Li P (2022) Endothelial cell-specific molecule 1 drives cervical cancer progression. Cell Death Dis 13:1043
doi: 10.1038/s41419-022-05501-5 pubmed: 36522312 pmcid: 9755307
Yang J, Yang Q, Yu S, Zhang X (2005) Endocan: a new marker for cancer and a target for cancer therapy. Biomed Rep 3:279–283
doi: 10.3892/br.2015.438
Cui Y, Guo W, Li Y, Shi J, Ma S, Guan F (2021) Pan-cancer analysis identifies ESM1 as a novel oncogene for esophageal cancer. Esophagus 18:326–338
doi: 10.1007/s10388-020-00796-9 pubmed: 33175267
Kano K, Sakamaki K, Oue N, Kimura Y, Hashimoto I, Hara K, Maezawa Y, Aoyama T, Fujikawa H, Hiroshima Y, Yamada T, Tamagawa H, Yamamoto N, Ogata T, Cho H, Ito H, Shiozawa M, Yukawa N, Yoshikawa T, Morinaga S, Rino Y, Yasui W, Masuda M, Miyagi Y, Oshima T (2020) ESM-1 gene expression on outcomes in stage II/III gastric cancer patients who received adjuvant S-1 chemotherapy. Vivo 34:461–467
doi: 10.21873/invivo.11796
Durston AJ, Timmermans JP, Hage WJ, Hendriks HF, de Vries NJ, Heideveld M, Nieuwkoop PD (1989) Retinoic acid causes an anteroposterior transformation in the developing central nervous system. Nature 340:140–144
doi: 10.1038/340140a0 pubmed: 2739735
Means A, Gudas LJ (1995) The roles of retinoids in vertebrate development. Annu Rev Biochem 64:210–233
doi: 10.1146/annurev.bi.64.070195.001221
Petkovich M, Brand NJ, Krust A, Chambon P (1987) A human retinoic acid receptor which belongs to the family of nuclear receptors. Nature 330:444–450
doi: 10.1038/330444a0 pubmed: 2825025
Osanai M, Sawada N, Lee GH (2010) Oncogenic and cell survival properties of the retinoic acid metabolizing enzyme, CYP26A1. Oncogene 29:1135–1144
doi: 10.1038/onc.2009.414 pubmed: 19935721
Osanai M (2017) Cellular retinoic acid bioavailability in various pathologies and its therapeutic implication. Pathol Int 67:281–289
doi: 10.1111/pin.12532 pubmed: 28422378
Osanai M, Takasawa A, Takasawa K, Kyuno D, Ono Y, Magara K (2023) Retinoic acid metabolism in cancer: potential feasibility of retinoic acid metabolism blocking therapy. Med Mol Morphol 56:1–10
doi: 10.1007/s00795-022-00345-6 pubmed: 36592231
Van heusden J, Wouters W, Ramaekers FC, Krekels MD, Dillen L, Borgers M, Smets G, (1998) The antiproliferative activity of all-trans-retinoic acid catabolites and isomers is differentially modulated by liarozole-fumarate in MCF-7 human breast cancer cells. Br J Cancer 77:1229–1235
doi: 10.1038/bjc.1998.207 pubmed: 9579827
Sonneveld E, van den Brink CE, van der Leede BM, Schulkes RK, Petkovich M, van der Burg B, van der Saag PT (1998) Human retinoic acid (RA) 4-hydroxylase (CYP26) is highly specific for all-trans-RA and can be induced through RA receptors in human breast and colon carcinoma cells. Cell Growth Diff 9:629–637
pubmed: 9716180
Iaassen I, Brakenhoff RH, Smeets SJ, Snow GB, Braakhuis BJ (2001) Metabolism and growth inhibition of four retinoids in head and neck squamous normal and malignant cells. Br J Cancer 85:630–635
doi: 10.1054/bjoc.2001.1952
Ozpolat B, Mehta K, Tari AM, Tari AM, Lopez-Berestein G (2002) All-trans-retinoic acid-induced expression and regulation of retinoic acid 4-hydroxylase (CYP26) in human promyelocytic leukemia. Am J Hematol 70:39–47
doi: 10.1002/ajh.10099 pubmed: 11994980
Shelton DN, Sandoval IT, Eisinger A, Chidester S, Ratnayake A, Ireland CM, Jones DA (2006) Up-regulation of CYP26A1 in adenomatous polyposis coli-deficient vertebrates via a WNT-dependent mechanism: implications for intestinal cell differentiation and colon tumor development. Cancer Res 66:7571–7577
doi: 10.1158/0008-5472.CAN-06-1067 pubmed: 16885356
WHO Classification of Tumours Editorial Board 2020 Female genital tumours. International Agency for Research on Cancer (WHO classification of tumours Lyon series, 5th ed.; vol.4)
Kanda Y (2013) Investigation of the freely available easy-to-use software ‘EZR’ for medical statistics. Bone Marrow Transpl 48:452–458
doi: 10.1038/bmt.2012.244
Straight SW, Hinkle PM, Jewers RJ, McCance DJ (1993) The E5 oncoprotein of human papilloma virus type 16 transforms fibroblasts and effects the downregulation of the epidermal growth factor receptor in keratinocytes. J Virol 67:4521–4532
doi: 10.1128/jvi.67.8.4521-4532.1993 pubmed: 8392596 pmcid: 237836
Nagy A, Munkacsy G, Gyorffy B (2021) Pancancer survival analysis of cancer hallmark genes. Sci Rep 11:6047
doi: 10.1038/s41598-021-84787-5 pubmed: 33723286 pmcid: 7961001

Auteurs

Midori Sato (M)

Department of Pathology, Sapporo Medical University School of Medicine, South-1, West-17, Chuo-Ku, Sapporo, 060-0061, Japan.
Cardiovascular Department, Jichi Medical University Saitama Medical Center, Saitama, 330-8503, Japan.

Ayano Inoue (A)

Department of Pathology, Sapporo Medical University School of Medicine, South-1, West-17, Chuo-Ku, Sapporo, 060-0061, Japan.

Akira Takasawa (A)

Department of Pathology, Sapporo Medical University School of Medicine, South-1, West-17, Chuo-Ku, Sapporo, 060-0061, Japan.

Kumi Takasawa (K)

Department of Pathology, Sapporo Medical University School of Medicine, South-1, West-17, Chuo-Ku, Sapporo, 060-0061, Japan.

Daisuke Kyuno (D)

Department of Pathology, Sapporo Medical University School of Medicine, South-1, West-17, Chuo-Ku, Sapporo, 060-0061, Japan.

Yusuke Ono (Y)

Department of Pathology, Sapporo Medical University School of Medicine, South-1, West-17, Chuo-Ku, Sapporo, 060-0061, Japan.

Kazufumi Magara (K)

Department of Pathology, Sapporo Medical University School of Medicine, South-1, West-17, Chuo-Ku, Sapporo, 060-0061, Japan.

Makoto Osanai (M)

Department of Pathology, Sapporo Medical University School of Medicine, South-1, West-17, Chuo-Ku, Sapporo, 060-0061, Japan. osanaim@sapmed.ac.jp.

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