In:
Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 5008-5008
Abstract:
Background and aims: Deleted in esophageal cancer1 (DEC1) is a frequently down-regulated candidate tumor suppressor gene in esophageal cancer (EC). We previously showed that this gene can suppress tumor growth and up-regulate Dual specificity phosphatase 6 (DUSP6), as a downstream target of DEC1, in esophageal squamous cell carcinoma (ESCC). In this study, we attempt to detect the expression of DEC1 during cancer progression and to identify subcellular localization of DEC1. We also evaluated the tumor suppressive role of DUSP6 in tumor development. Methods: As yet, there are no other published studies of DEC1 protein. Thus, DEC1-specific polyclonal antibody was generated and utilized for Western blotting, tissue microarray study, and immunostaining. We utilized cell functional assays such as colony formation, cell proliferation, and wound healing assays, as tools to evaluate tumor suppressive role of DUSP6. Results: Loss of DEC1 expression is observed in ESCC tumors, as compared to their matched normal counterparts in Western blot analysis. Significant loss of DEC1 during cancer progression was found. The expression of DEC1 is significantly related to cancer family history and age of patients. By immunostaining, DEC1 was localized to the cytoplasm, nucleus, and perinuclear region. In addition, we observed an important role of DUSP6 in suppressing cell growth and migration. Conclusions: We further validated the crucial role of DEC1 expression in EC tumorigenesis by use of tissue microarray. We identified subcellular localization of DEC1, providing a basis for further study of the tumor suppressive mechanism of DEC1. In addition, a tumor suppressive role of DUSP6 was confirmed. 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 5008.
Type of Medium:
Online Resource
ISSN:
0008-5472
,
1538-7445
DOI:
10.1158/1538-7445.AM10-5008
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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