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Carbonic Anhydrase IX Is Highly Expressed in Hereditary Nonpolyposis Colorectal Cancer

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Carbonic Anhydrase IX Is Highly Expressed in Hereditary Nonpolyposis Colorectal Cancer 1760 Carbonic Anhydrase IX Is Highly Expressed in Hereditary Nonpolyposis Colorectal Cancer Anssi M. Niemela¨,3,4 Piritta Hynninen,5 Jukka-Pekka Mecklin,1 Teijo Kuopio,2 Antti Kokko,7 Lauri Aaltonen,7 Anna-Kaisa Parkkila,6 Silvia Pastorekova,8 Jaromir Pastorek,8 Abdul Waheed,9 William S. Sly,9 Torben F. Ørntoft,10 Mogens Kruhøffer,10 Hannu Haapasalo,4 Seppo Parkkila,3 and Antti J. Kivela¨1 Departments of 1Surgery and 2Pathology, Jyva¨skyla¨Central Hospital, Jyva¨skyla¨, Finland; 3Institute of Medical Technology and Departments of 4Pathology, 5Obstetrics and Gynecology, and 6Neurology, University of Tampere and Tampere University Hospital, Tampere, Finland; 7Department of Medical Genetics and Cancer Biology Research Program, University of Helsinki, Helsinki, Finland; 8Center of Molecular Medicine, Institute of Virology, Slovak Academy of Sciences, Bratislava, Slovak Republic; 9Department of Biochemistry and Molecular Biology, Saint Louis University School of Medicine, St. Louis, Missouri; and 10Department of Clinical Biochemistry, Aarhus University Hospital, Skejby, Aarhus N, Denmark Abstract Carbonic anhydrase (CA) II, CA IX, and CA XII are HNPCC group. For more information, 77 specimens expressed in various neoplasias and have been linked to were immunohistochemically stained to study the levels tumorigenesis. We examined their expression in three of CA II, CA IX, and CA XII. Immunohistochemical different groups of colorectal cancer [i.e., microsatellite analyses further confirmed that the subgroups express stable (MSS), microsatellite instable (MSI), and hered- CA II, CA IX, and CA XII differentially, and the HNPCC itary nonpolyposis colorectal cancer (HNPCC)]. First, we tumors express high levels of CA IX. Expression of analyzed gene expression profiles of 113 specimens by a these CAs did not correlate to Dukes stage or grade of microarray method to study the expression of various differentiation. Our results show that CAs are differen- CA isozymes in the subgroups of colorectal cancer. The tially expressed in the subgroups of colorectal cancer, results indicated that mRNAs for CA II and CA XII are and CA IX expression seems to be very high in most down-regulated and CA IX mRNA is up-regulated in all cases of HNPCC. CA IX could be a potential diagnostic three tumor categories when compared with the normal and therapeutic target in HNPCC. (Cancer Epidemiol tissue. The up-regulation of CA IX was greatest in the Biomarkers Prev 2007;16(9):1760–6) Introduction Colorectal cancer is diagnosed in f150,000 people in endometrium, ovary, stomach, small intestine, hepato- the United States and 500,000 worldwide each year (1). biliary tract, ureter, and renal pelvis. From all cases, about 3% to 4% are linked to the familial Genetic instability, which is common in colorectal cancer syndromes. The most common form is hereditary cancer and often targets the DNA mismatch repair genes, nonpolyposis colorectal cancer (HNPCC; also called the is one hallmark of carcinogenesis and can be promoted Lynch syndrome), which is caused by a germ-line by cell stress factors within the tumor microenvironment mutation in one of four DNA mismatch repair genes. such as cell hypoxia (5). What is less known is the However, many colorectal cancers show microsatellite mechanism through which hypoxia contributes to genet- instability without evidence of germ-line abnormalities ic instability (6). The transcription factor called hypoxia- (2). In these cases, the cause is biallelic methylation of inducible factor (HIF)-1a is crucial for the cellular the promoter sequences of MLH1—an epigenetic, not response to hypoxia and is frequently overexpressed in inherited, change that leads to a deficiency of DNA hypoxic regions of human cancers, resulting in activation mismatch repair (2). The prognosis for HNPCC is better of genes essential for cell survival. One of these HIF- than for the sporadic form of cancer (3, 4), although the inducible genes is called CA9,whichencodesthe patients with HNPCC have an increased risk for cancer carbonic anhydrase (CA) IX isozyme that is over- development in certain extracolonic sites such as the expressed in certain carcinomas (7, 8). CA XII is another member of the CA isozyme family that has been reported to be inducible by hypoxia (8), although the evidence is Received 1/27/07; revised 6/12/07; accepted 6/14/07. not yet as convincing as for CA IX. Grant support: Sigrid Juselius Foundation, Academy of Finland, Finnish Cancer CAs have been classically considered zinc-containing Foundation, Finnish Cultural Foundation, Slovak Grant Agencies VEGA (2/3055 and metalloenzymes, which catalyze a very fundamental APVV-51-024805) and NIH (DK40163). chemical reaction wherein carbon dioxide is hydrated The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance to carbonic acid, which then dissociates to bicarbonate X X + À with 18 U.S.C. Section 1734 solely to indicate this fact. and proton (CO2 +H2O H2 CO3 H + HCO3 ). There Requests for reprints: Antti J. Kivela¨, Department of Surgery, Jyva¨skyla¨Central are at least 13active a-CA isozymes in mammals Hospital, Keskussairaalantie 19, 40620 Jyva¨skyla¨, Finland. Phone: 358-50-324-7762; Fax: 011-358-14-269-3626. E-mail: [email protected] including five cytoplasmic (CA I, CA II, CA III, CA VII, Copyright D 2007 American Association for Cancer Research. and CA XIII), two mitochondrial (CA VA and CA VB), doi:10.1158/1055-9965.EPI-07-0080 one secreted (CA VI), and five membrane-associated Cancer Epidemiol Biomarkers Prev 2007;16(9). September 2007 Downloaded from cebp.aacrjournals.org on October 4, 2021. © 2007 American Association for Cancer Research. Cancer Epidemiology, Biomarkers & Prevention 1761 (CA IV, CA IX, CA XII, CA XIV, and CA XV) forms. The detectable levels in majority (>50%) of the samples, discovery that some of the CA isozymes (CA II, CA IX, which were removed from further analyses (22). and CA XII) are implicated in tumorigenesis has ignited a completely new era in CA research during the past Tumor Samples for Immunohistochemistry. Tumor decade (7, 9–12). Colorectal cancer was one of the first samples were collected together with routine histopath- tumor types wherein CA expression was explored in ologic specimens taken during surgical operations in detail (13–15). It has been shown that CA II is down- Jyva¨skyla¨Central Hospital between 1979 and 2004. The regulated and CA IX is up-regulated in the tumor study was approved by the Ethics Committee of the tissue compared with the normal intestinal epithelium Jyva¨skyla¨ Central Hospital. The samples included in (14, 16, 17). CA XII levels remained quite constant during the immunohistochemical staining were not the same the colorectal tumor progression, although the distribu- tumors that were studied by the microarray analyses. tion of the enzyme became more widespread, in contrast There were 77 colorectal tumor samples, including to its confined expression in the normal mucosa (15). 43MSS, 18 MSI, and 16 HNPCC. The histologic grade Tumor-associated CAs may participate in oncogenesis by was low in 29 lesions, moderate in 26 lesions, and high acidifying the extracellular milieu adjacent to cancer in 8 lesions. The lesions had been isolated from the cells. This acidification would create a microenvironment ascending colon (N = 10), transverse colon (N = 4), within the tumor that would be conducive to cancer descending colon (N = 2), sigmoid colon (N = 10), rectum growth and spread (18, 19). Although the exact mecha- (N = 19), and rectosigmoideum (N = 1). Additional 14 nisms are largely unknown, acidification has been linked samples were obtained from the colon, but the informa- to various events of tumor progression such as defective tion about the exact location was not available. Of the intercellular adhesion, increased invasion, and up-regu- carcinomas, 14 were at Dukes stage A, 28 at stage B, lation of growth factors and matrix metalloproteinases. 16 at stage C, and 3at stage D. Interestingly, acidification seems to contribute to the increase in mutation rate and reduction in DNA repair Immunohistochemistry. Tissue samples were washed (20)—both being cardinal features of genetic instability. briefly with PBS, fixed with 4% neutral-buffered form- It is plausible to predict that CAs, as the major pH- aldehyde, and embedded in paraffin. Sections were cut at A regulating enzymes, are involved in modulating pH in 5 m and placed on SuperFrost Plus microscope slides tumor microenvironments. This hypothesis was strongly (Menzel). Immunoperoxidase staining was done using supported by recent observations that CA IX contributes an automated Lab Vision Autostainer 480 (Immuno- to the acidification process in cells that are cultured Vision Technologies Co.). under hypoxic conditions (21). The polyclonal rabbit antibodies against human CA II The aim of this study was to obtain a comprehensive and XII have previously been characterized and pro- view of CA expression in different groups of colorectal duced (15, 23, 24). The monoclonal antibody M75 cancer including microsatellite stable (MSS) and micro- against human CA IX has also been described previously satellite instable (MSI) sporadic carcinomas and HNPCC. (15, 23, 25). In the first part of the study, we analyzed mRNA The automated immunostaining was done using expression levels of multiple CA isozymes in colorectal Power Vision+ Poly-HRP IHC Kit (ImmunoVision cancers using an expression microarray technology. Technologies Co.) reagents and included the following Thereafter, we studied CA II, CA IX, and CA XII steps: (a) rinsing in wash buffer; (b) treatment in 3% expression in MSS, MSI, and HNPCC colorectal tumors H2O2 in double-distilled water for 5 min and rinsing with by immunohistochemistry. To the best of our knowledge, wash buffer; (c) blocking with cow colostrum diluted 1:2 this is the first study on CA expression in hereditary in TBS containing 0.05% Tween 20 for 30 min and rinsing colorectal cancer and the first correlation of CAs to the in wash buffer; (d) incubation with primary antibody genetic stability/instability in any cancer.
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