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Estrogen Receptor–Binding Fragment–Associated Antigen 9 Is a Tumor-Promoting and Prognostic Factor for Renal Cell Carcinoma

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Estrogen Receptor–Binding Fragment–Associated Antigen 9 Is a Tumor-Promoting and Prognostic Factor for Renal Cell Carcinoma Research Article Estrogen Receptor–Binding Fragment–Associated Antigen 9 Is a Tumor-Promoting and Prognostic Factor for Renal Cell Carcinoma Tetsuo Ogushi,1 Satoru Takahashi,1 Takumi Takeuchi,1 Tomohiko Urano,2 Kuniko Horie-Inoue,3 Jinpei Kumagai,1 Tadaichi Kitamura,1 Yasuyoshi Ouchi,2 Masami Muramatsu,3 and Satoshi Inoue2,3 Departments of 1Urology and 2Geriatric Medicine, Faculty of Medicine, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan and 3Research Center for Genomic Medicine, Saitama Medical School, Yamane, Hidaka-shi, Saitama, Japan Abstract target organs as well as several other tissues such as brain, liver, The estrogen receptor–binding fragment–associated antigen and kidney (2). The protein expression of EBAG9 is estrogen inducible, as it has been shown in ovariectomized mice treated 9(EBAG9) has been identified as a primary estrogen- h responsive gene in human breast cancer MCF7 cells. A high with 17 -estradiol administration (2). The physiologic function of expression of EBAG9 has been observed in invasive breast EBAG9 has not been well defined, yet the molecule may be cancer and advanced prostate cancer, suggesting a tumor- implicated in cancer pathophysiology, with several lines of evidence promoting role of the protein in malignancies. Here we show of the protein expression in malignancies, including breast (3), that intratumoral (i.t.) administration of small interfering ovarian (4), prostate (5), and hepatocellular carcinomas (6). In RNA against EBAG9 exerted overt regression of tumors prostate cancer (5), EBAG9 expression significantly correlated with following s.c. implantation of murine renal cell carcinoma advanced pathologic stages and high Gleason score (P = 0.0305 and P < 0.0001, respectively), suggesting the abundance of EBAG9 may (RCC) Renca cells. Overexpression of EBAG9 did not promote the proliferation of culture Renca cells; however, the relate to the progression of malignant tumors. inoculated Renca cells harboring EBAG9 (Renca-EBAG9) in In the present study, we investigated whether EBAG9 expression BALB/c mice grew faster and developed larger tumors is critical in tumor development of renal cell carcinoma (RCC). compared with Renca cells expressing vector alone (Renca- RCC that comprises the majority of kidney cancer is one of the 10 vector). After renal subcapsular implantation, Renca-EBAG9 most common malignancies in industrialized countries (7). The tumors significantly enlarged compared with Renca-vector prognosis of patients with advanced RCC is poor, as 5-year survival tumors in BALB/c mice, whereas both Renca-EBAG9 and rate is <5% (8), and the treatment of metastatic RCC remains a Renca-vector tumors were developed with similar volumes in difficult clinical challenge. Development of new and alternative BALB/c nude mice. No apparent difference was observed in modalities of diagnosis and therapy for RCC is a clinical requisite. specific cytotoxic T-cell responses against Renca-EBAG9 and We used murine syngeneic renal adenocarcinoma model of Renca Renca-vector cells; nonetheless, the number of infiltrating cells in this study and investigated whether gene silencing or CD8+ T lymphocytes was decreased in Renca-EBAG9 subcap- overexpression of EBAG9 influences Renca cell growth and/or in vivo tumorigenesis. Administration of small interfering RNA sular tumors. Furthermore, immunohistochemical study of EBAG9 in 78 human RCC specimens showed that intense and (siRNA) against EBAG9 regressed s.c. Renca tumors. The prolifer- diffuse cytoplasmic immunostaining was observed in 87% of ation of culture Renca cells constitutively expressing EBAG9 was the cases and positive EBAG9 immunoreactivity was closely not basically different from control Renca cells, whereas EBAG9- correlated with poor prognosis of the patients. Multivariate expressing cells grew faster in BALB/c mice and developed larger tumors. The tumor-promoting effect of EBAG9 in Renca tumors analysis revealed that high EBAG9 expression was an + independent prognostic predictor for disease-specific survival may relate to the suppression of antitumor immunity, as i.t. CD8 T (P = 0.0485). Our results suggest that EBAG9 is a crucial lymphocytes were reduced in renal subcapsular Renca tumors. The regulator of tumor progression and a potential prognostic tumorigenic relevance of EBAG9 in Renca models further extended marker for RCC. (Cancer Res 2005; 65(9): 3700-6) to clinicopathologic significance of the molecule in human RCC. EBAG9 immunoreactivity was closely correlated with poor prognosis of the patients and it was an independent prognostic Introduction predictor for disease-specific survival. Our findings show that Estrogen receptor–binding fragment associated gene 9 (EBAG9) EBAG9 is a tumor-promoting factor and a potential prognostic is an estrogen-responsive gene that we previously identified in marker in RCC. MCF-7 human breast carcinoma cell line using a CpG-genomic binding site cloning method (1). EBAG9 protein, whose molecular size is 32 kDa by Western blot analysis, is expressed in estrogen Materials and Methods Reagents. Rabbit anti-EBAG9 polyclonal antibody was generated against a fusion protein of glutathione S-transferase and EBAG9 (2). Rabbit Note: Supplementary data for this article are available at Cancer Research Online polyclonal antihuman CD3 antibody (DakoCytomation, Carpinteria, CA), rat (http://cancerres.aacrjournals.org/). antimouse CD4 (L3T4; clone RM 4-5), rat antimouse CD8a (Ly-2; 53-6.7) Requests for reprints: Satoshi Inoue, Department of Geriatric Medicine, monoclonal antibodies (BD PharMingen, San Diego, CA), and anti–h-actin Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, monoclonal antibody (Sigma, St. Louis, MO) were commercially purchased. Tokyo 113-8655, Japan. Phone: 81-3-5800-8652; Fax: 81-3-5800-6530; E-mail: INOUE- [email protected]. Human EBAG9 cDNA was cloned into a mammalian expression vector I2005 American Association for Cancer Research. pcDNA3 (Invitrogen, Carlsbad, CA). Cancer Res 2005; 65: (9). May 1, 2005 3700 www.aacrjournals.org Downloaded from cancerres.aacrjournals.org on September 24, 2021. © 2005 American Association for Cancer Research. EBAG9 as a Tumor-Promoting Factor for RCC Tumor cells. Renca is a spontaneously arising murine RCC and was subcapsule of the left kidney of BALB/c wild-type and nude mice. Mice were prepared as previously described (9, 10). Tumor cells were maintained in sacrificed 25 days after implantation and tumors were excised. RPMI 1640 containing 10% FCS and antibiotics. Cell proliferation assay. Cells were seeded at a density of 1 to 3 Â 105 Mice. BALB/c mice and BALB/c nu/nu mice (Nisseizai, Tokyo, Japan) cells per dish into 10-cm dishes and hemocytometer counting was done that were syngeneic to Renca cells were kept under specific pathogen-free every 2 days. Doubling time during exponential growth was determined by a conditions and fed dry food and water. All mice used for experiments were formula: [incubation time (h) Â log102] / [log10(cell number at sampling male at the age of 5 weeks. period) À log10(plating cell number)] (12). Patients and tissue preparation. We investigated 78 tissue samples of Proliferation assays were done using the 2-(2-methoxy-4-nitrophenyl)-3- RCC obtained from patients (14 females and 64 males) who underwent (4-nitrophenyl)-5-(2,4-disulfophenyl)-2H tetrazolium monosodium salt radical or partial nephrectomy at Tokyo University Hospital between 1990 (WST-8) reagent (Nacalai, Kyoto, Japan; ref. 13). The assay is based on and 1995. Patient information was retrieved from the review of patient the conversion of the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium charts. Staging and grading of the tumors were done according to the 1997 bromide (MTT)-like tetrazolium salt WST-8 to a water-soluble formazan International Union Against Cancer tumor-node-metastasis classification by metabolically active cells and provides a quantitative determination of and WHO histopathologic typing, respectively (11). The mean age of this viable cells. Cells were seeded in 96-well plates at an initial density of 625 population was 54 years (26-76 years) and the mean follow-up period was to 5,000 cells per well. At 1 hour after inoculation, cells were transfected 60 months (2-78 months). For 32 patients with advanced tumors (pT2 or with either EBAG9 siRNA or Scramble II Duplex (100 ng per well) using greater), adjuvant therapy was done, including immune therapy (n = 30), GeneSilencer reagent (Gene Therapy Systems). Assays were done on days 0, radiation (n = 5), and surgery for metastatic diseases in lung, colon, and 2, and 4. For cells cultured up to day 4, medium was once exchanged on pancreas (n = 8). During the follow-up period, 55 patients (70.5%) survived day 2. Spectrophotometric absorbance at 450 nm (for formazan dye) was without evidence of disease, eight cases (10.3%) presented with tumor measured with absorbance at 620 nm for reference. recurrence, and 15 cases (19.2%) died of disease. None died of other Cytotoxicity assay. Renca-EBAG9 or Renca-vector cells were used as diseases. target cells. Splenocytes of Renca-bearing BALB/c mice were stimulated for Western blot analysis. Cells were lysed in radioimmunoprecipitation 5 days in vitro with irradiated Renca cells at a splenocyte/tumor cell ratio of assay buffer [50 mmol/L Tris-HCl (pH 8.0), 200 mmol/L NaCl, 20 mmol/L 20:1 in the presence of 1,000 IU/mL interleukin-2 and used as effector CTLs. NaF2, 2 mmol/L EGTA, 1 mmol/L DTT, 2 mmol/L sodium vanadate, 0.5% Target cells were incubated with effector CTLs at various E/T ratios in a v/v NP40 supplemented with a protease inhibitor cocktail Complete final volume of 200 AL for 18 hours at 37jC. Lactate dehydrogenase release (Boehringer Manheim GmbH, Mennheim, Germany)]. Proteins were from cells with a damaged membrane was examined using CytoTox-ONE resolved by 12.5% SDS-PAGE and transferred to polyvinylidene difluoride Reagent (Promega, Madison, WI) and fluorescence was measured with an membranes.
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