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Cellular and Molecular Biology

Abstract 4998: Down-regulation of Hsulf-1 promotes tumorigenicity of ovarian cancer cells

Xiaoping He, Tsuyoshi Ohta and Viji Shridhar
Xiaoping He
1Mayo Clinic College of Medicine, Rochester, MN.
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Tsuyoshi Ohta
1Mayo Clinic College of Medicine, Rochester, MN.
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Viji Shridhar
1Mayo Clinic College of Medicine, Rochester, MN.
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DOI: 10.1158/1538-7445.AM10-4998 Published April 2010
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Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC

Abstract

Human Sulfatase1 enzyme (HSulf-1) is down-regulated in a majority of ovarian cancer cell lines and primary tumors, but the functional consequence of this downregulation remains unclear. Here, we showed that down-regulation of HSulf-1 by RNA interference in OV202 ovarian cancer cells resulted in an elevated level of phosphorylated AKT. Conversely, over-expression of HSulf-1 in SKOV3 ovarian cancer cells led to decreased phosphorylation of AKT. When cells were treated with CDDP, OV202 cells with knockdown of HSulf-1 displayed more resistance to drug-induced apoptosis, with IC50 value 3-fold higher than cells with non-targeting shRNA, while SKOV3 cells with overexpression of HSulf-1 were more sensitive to drug-induced apoptosis compared to the control cells. Moreover, knockdown of HSulf-1 also endowed ovarian cancer cells with increased resistance to detachment-induced apoptosis (anoikis). Cell proliferation assays revealed that knockdown of HSulf-1 significantly accelerated cell proliferation of ovarian cancer cells in vitro. Importantly, when cells were injected subcutaneously, 7 of 8 (87.5%) nude mice developed tumors with HSulf-1 knockdown cells within 2 weeks. However, none of the mice injected with nontargeted control transduced cells (control group) developed tumors. Four weeks after injection, 8 of 8 (100%) nude mice developed tumors with HSulf-1 down-regulated cells, while only 2 of 5 (40%) mice had tumors in the control group. The average tumor weight was 4.2±2.7g per mice in HSulf-1 knockdown group, significantly higher than 0.6±0.3g per mice in the control group. Collectively, these results strongly suggest that down-regulation of HSulf-1 promotes tumorigenicity of ovarian cancer possibly due to elevated activation of AKT pathway.

Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend.

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 4998.

  • ©2010 American Association for Cancer Research
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Cancer Research: 70 (8 Supplement)
April 2010
Volume 70, Issue 8 Supplement
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Abstract 4998: Down-regulation of Hsulf-1 promotes tumorigenicity of ovarian cancer cells
Xiaoping He, Tsuyoshi Ohta and Viji Shridhar
Cancer Res April 15 2010 (70) (8 Supplement) 4998; DOI: 10.1158/1538-7445.AM10-4998

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Abstract 4998: Down-regulation of Hsulf-1 promotes tumorigenicity of ovarian cancer cells
Xiaoping He, Tsuyoshi Ohta and Viji Shridhar
Cancer Res April 15 2010 (70) (8 Supplement) 4998; DOI: 10.1158/1538-7445.AM10-4998
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Cancer Research Online ISSN: 1538-7445
Cancer Research Print ISSN: 0008-5472
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