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  • American Association for Cancer Research (AACR)  (3)
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  • American Association for Cancer Research (AACR)  (3)
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  • 1
    Online Resource
    Online Resource
    Abstract 235: Desmocollin 2 (DSC2), identified by CAST method, is associated with intestinal phenotype of gastric cancer
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 235-235
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 235-235
    Abstract: Gastric cancer (GC) is one of the most common human cancers. Identification of novel genes encoding secreted or transmembrane proteins expressed specifically in GC is important for the development of ideal biomarkers for cancer diagnosis and therapeutics. In the present study, we tried to identify genes encoding cell surface and secretory proteins in GC using Escherichia coli ampicillin secretion trap (CAST) method. CAST libraries were generated from two GC cell lines, MKN-1 and MKN-28. Ampicillin-resistant 1,440 colonies from each library were sequenced and these sequences were compared to the public databases using BLAST (NCBI). Many genes encoding secreted and transmembrane proteins including some known genes were identified. Quantitative RT-PCR was performed to confirm the overexpression of the candidate genes in GC, and the expressions of several genes are narrowly restricted in GC. Among these genes, we focused on the desmosomal cadherin desmocollin 2 (DSC2). DSC2 is ubiquitously expressed in several normal tissues where desmosomes exist. In cancers, the reduction of DSC2 in sporadic colorectal cancer is reported as desmocollin switching. It is also known that the homeodomain transcription factors Cdx1 and Cdx2 regulate DSC2 expression in colon cancer cells. Quantitative RT-PCR analyses with 14 kinds of normal tissues and 9 GC cases showed that DSC2 is highly expressed in GCs. In normal tissues, the expression was seen in the heart and pancreas at the lower levels, but not in the stomach. Overexpression of DSC2 was observed in 13 (31%) of 41 GC cases. Immunohistochemical analyses revealed that DSC2 was preferentially expressed in the cases with mucosal or submucosal invasion. DSC2 expression was significantly associated with the well differentiated cases. There were no correlations between DSC2 expression and lymph node metastasis, pathological stage, or overall survival. Additionally, DSC2 was significantly associated in GCs positive for MUC2 and CDX2. Cell invasion assay and MTT assay revealed that knockdown for DSC2 of GC cell lines by siRNA did not inhibit either cell growth or invasion ability. These findings suggest that DSC2 is involved in GC with intestinal differentiation. DSC2 is a good biomarker of intestinal type GC. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 235.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM10-235
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 2
    Online Resource
    Online Resource
    Abstract 3186: The role of fibroblast growth factor 9 for androgen-independent growth of prostate cancer cells
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 3186-3186
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 3186-3186
    Abstract: Introduction & Objectives: In prostate tissue, impairment of communication between epithelial and stromal cells through fibroblast growth factor 9 (FGF9) signaling pathway has been thought to cause failure of tissue homeostasis and development of malignant disease. Previous studies have reported that FGF9 expression increased in the prostate cancer xenografts derived from bone metastasis. The aim of our study is to investigate the role of FGF9 for progression of prostate cancer. Material & Methods: Immunohistochemical staining using anti-FGF9 antibody were performed for tissues derived from radical prostatectomy for 98 male patients. Cell viability and apoptosis of DU145, LNCaP and androgen-independent LNCaP subline (AI-LNCaP) were assessed with MTT assay and with Apopercentage apoptosis assay in the presence or absence of treatment with recombinant FGF9 or anti-FGF9 neutralizing antibody, respectively. Results: In immunohistochemical staining, FGF9 positive cells were detected in 12 samples. In cases with Gleason score 8 or higher, rates of cases with FGF9 positive cells were 32.1%, significantly higher than those in case with Gleason score 6 (3.3%, p=0.016) and 7 (5.0%, p=0.0079), respectively. 5-year biochemical relapse-free survival rate in cases with FGF9 positive cells were 31.3%, significantly lower than those in cases that FGF9 positive cells were not detectable (77.6%, p=0.0008). In condition with androgen-deprivated medium, cell viability of LNCaP was significantly lower than that of AI-LNCaP, and enhanced to the same level by treatment with FGF9. Furthermore, cell viability of AI-LNCaP and DU145 were significantly suppressed by treatment with anti-FGF9 neutralizing antibody. Significantly more apoptotic cells were detected in LNCaP than in AI-LNCaP by androgen deprivation, and decreased to same level as in AI-LNCaP by treatment with FGF9. Conclusions: These results indicate that FGF9 can contribute for progression of prostate cancer through stimulation for cell proliferation and anti-apoptotic effect. FGF9 may be candidates of novel therapeutic targets for hormone-refractory prostate cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 3186.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM10-3186
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
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  • 3
    Online Resource
    Online Resource
    Abstract 242: Analyses of novel genes encoding secreted and transmembrane proteins identified by CAST method: CDON is highly expressed in prostate cancer
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Research Vol. 70, No. 8_Supplement ( 2010-04-15), p. 242-242
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 242-242
    Abstract: Prostate cancer (PCa) is one of the most common human cancers. Identification of novel genes that encode membrane-spanning or secreted proteins expressed specifically in PCa has a great advantage to develop of ideal biomarkers for cancer diagnosis and therapeutics. Escherichia coli Ampicillin Secretion Trap (CAST) is a signal sequence trap method to identify genes encoding cell surface and secreted proteins. In this study, to identify novel diagnostic and therapeutic targets of PCa, CAST method was used. We generated cDNA libraries from normal prostate and two PCa cell lines, LNCaP and DU145. These CAST libraries were ligated into the pCAST which was plasmid with a mutant beta-lactamase lacking the endogenous signal peptide. Survival on ampicillin was observed only when various cDNA fragments encoding a signal sequence were inserted. We sequenced 960 ampicillin-resistant colonies for normal prostate CAST library, 1344 colonies for LNCaP CAST library and 960 colonies for DU145 CAST library. By comparing these sequences to those deposited in the public databases using BLAST (NCBI), 223 genes from normal prostate CAST library, 234 genes from LNCaP and 228 genes from DU145 were identified. To extract highly expressed genes in PCa, the genes expressed in normal prostate were excluded. Quantitative RT-PCR analyses of 64 candidate genes were performed and compared mRNA levels in 9 PCa tissues, 2 normal prostate tissues and 14 kinds of normal tissues. Quantitative RT-PCR analyses revealed that CDON was highly expressed in PCa. Overexpression of CDON (tumor/normal ratio & gt; 2) was observed in 8 (89%) of 9 PCa tissues. CDON is a cell surface receptor of the immunoglobulin /fibronectin type III repeat family. By western blot analysis, low to moderate CDON expression was noted in LNCaP cell extracts and moderate to high CDON expression was noted in DU145 cell extracts. The expression of CDON in LNCaP and DU145 was suppressed by treatment with CDON specific siRNA. Cell invasion assay and MTT assay revealed that knockdown of CDON in LNCaP cells did not inhibit both cell growth and invasion ability, but knockdown of CDON in DU145 cells inhibited both cell growth and invasion ability. In conculusion, CAST is a robust and rapid method to identify cell surface and secreted proteins. CDON was up-regulated in PCa and participated in cell growth and invasion. These finding suggest that CDON may be a good therapeutic target. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 242.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM10-242
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
    Location Call Number Limitation Availability
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    Online Resource
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