In:
Cancer Research, American Association for Cancer Research (AACR), Vol. 70, No. 8_Supplement ( 2010-04-15), p. 1052-1052
Abstract:
Basic fibroblast growth factor (FGF-2) is a potent wide-spectrum antiapoptotic mitogen, and the dysregulation of its expression is associated with cell proliferation and immortalization in a wide variety of tumors. We have previously reported that FGF-2 and NUDT6, the product of its antisense gene, are co-localized and inversely expressed in C6 glioma cells, and that constitutive overexpression of NUDT6 suppresses cellular FGF-2 expression, nuclear translocation, and the resumption of cell cycles (Baguma-Nibasheka et al., Mol Cell Endocrinol, 267:127-136, 2007). For the current report, we investigated the role of the endogenous RNAi machinery in mediating the post-transcriptional effects of NUDT6 on FGF-2 expression. FGF-2 knockdown was accompanied by a significant ( & gt;3 fold) increase in NUDT6 mRNA, and vice versa. Similar converse effects were observed on the cognate protein levels, as assessed by confocal immunoflourescence, Western blotting, and flow cytometry, indicating that these two transcripts may be mutually regulatory. Remarkably, knockdown of either transcript reduced cell proliferation and inhibited S-phase re-entry following serum deprivation (Table 1), indicating that both FGF-2 and NUDT6 may be involved in the regulation of cell cycle progression. Supported by the CIHR and NSERC.Table 1.S-Phase Percentages1 of C6 Cells following Knockdown and G0 Arrest.Hours after Return to 10% FBS Medium0361224Control siRNA4.8 ± 0.516.8 ± 1.321.6 ± 1.822.4 ± 1.123.0 ± 1.5NUDT6 siRNA4.1 ± 0.510.6 ± 1.3*14.2 ± 1.6*16.7 ± 1.8*19.8 ± 0.8FGF-2 siRNA3.5 ± 0.55.9 ± 0.8*6.9 ± 1.2*11.2 ± 1.1*14.5 ± 1.0*1mean ± SEM. * = significantly different from control; p & lt;0.05, n=3. 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 1052.
Type of Medium:
Online Resource
ISSN:
0008-5472
,
1538-7445
DOI:
10.1158/1538-7445.AM10-1052
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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