Abstract 256: Elucidating the role of ARID3B in ovarian cancer stem cells
Ovarian cancer is the fifth leading cause of cancer death among US women and accounts for more deaths than any other cancer of gynecological origin. In light of the lethality, it is critical to discover and understand the common molecular characteristics in ovarian cancer. Our lab demonstrated that...
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Veröffentlicht in: | Cancer research (Chicago, Ill.) Ill.), 2013-04, Vol.73 (8_Supplement), p.256-256 |
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Sprache: | eng |
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Zusammenfassung: | Ovarian cancer is the fifth leading cause of cancer death among US women and accounts for more deaths than any other cancer of gynecological origin. In light of the lethality, it is critical to discover and understand the common molecular characteristics in ovarian cancer. Our lab demonstrated that ARID3B, a member of the AT-rich interactive domain family of proteins, is overexpressed in ovarian cancer. Furthermore, ARID3B is essential for embryonic development and is present in embryonic stem cells. Overexpression of ARID3B in ovarian cancer cells leads to increased tumor growth and decreased survival in xenograft studies. Therefore, we hypothesize that ARID3B regulates cancer stem cell production, which enhances tumorigenesis. We have found that stem-cell marker CD133 is upregulated in ovarian cancer human cell line SKOV3IP overexpressing ARID3B. We are currently assessing the mechanism for ARID3B regulation of ovarian cancer stem cells using in vitro models. Determining the role of ARID3B in cancer stem cells may help us better understand the molecular mechanisms that regulate tumor initiation, chemoresistance, and ovarian cancer progression.
Citation Format: Victoria E. Deneke, Lynn Roy, Richard Dahl, Karen D. Cowden Dahl. Elucidating the role of ARID3B in ovarian cancer stem cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 256. doi:10.1158/1538-7445.AM2013-256 |
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ISSN: | 0008-5472 1538-7445 |
DOI: | 10.1158/1538-7445.AM2013-256 |