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The \Spot 14\ gene resides on the telomeric end of the 11q13 amplicon and is expressed in lipogenic breast cancers: Implications for control of tumor metabolism
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The \Spot 14\ gene resides on the telomeric end of the 11q13 amplicon and is expressed in lipogenic breast cancers: Implications for control of tumor metabolism
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The \Spot 14\ gene resides on the telomeric end of the 11q13 amplicon and is expressed in lipogenic breast cancers: Implications for control of tumor metabolism
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Dissertation
The \Spot 14\ gene resides on the telomeric end of the 11q13 amplicon and is expressed in lipogenic breast cancers: Implications for control of tumor metabolism
1999
Overview
Spot 14 (S14) is a ∼17 KD nuclear protein that functions at the transcriptional level to regulate de novo synthesis of fatty acids in liver, brown and white adipose, and. lactating mammary tissues. Localization of the S14 gene to. chromosome 11q13.5 suggested it may contribute to tumorigenes is in breast. In ∼15% of breast cancers, chromosome 11q13 is amplified and this predicts a poor prognosis. Although two candidate oncogenes from this region, CCND1 and EMS1, were identified, most studies suggest there are other cooperating oncogenes at 11q13. Overexpression of fatty acid synthase (FAS), a key lipogenic enzyme, occurs in a subset of breast cancers and also predicts a poor prognosis. Furthermore, pharmacologic inhibition of FAS in lipogenic tumors induced apoptosis. This raised the question of whether amplification of the S14 gene caused S14 overexpression and thereby stimulated tumor lipogenesis. The focus of this the.sis, was to determine whether S14 is part of the 11q13 amplicon and to characterize its potential role in the pathophysiology of breast cancer. The S14 gene was localized to between markers D11S906 and D11S937, at the telomeric end of the 11q13 amplicon and was amplified in 2/7 breast cancer cell lines. Expression of S14 was identified in 6/7 breast cancer cell lines. The cell line that did not express S14, MDA-MB-435s, was the only one with a relatively low rate of lipogenesis. Expression of S14 was also examined by immunohistochemistry. In normal breast, S14 expression only occurred when there was lactation. In 21 primary breast cancers, S14 was expressed in 67%, and acetyl-CoA carboxylase was expressed in 71%. The expression of S14 and ACC was 86% concordant. Expression of S14 was also induced by progesterone in T47D breast cancer cells. The induction occurred in close association with the degree and time course of FAS induction. These data supported the hypothesis that S14 is part of the 11q13 amplicon and that its expression causes increased tumor lipogenesis. Inhibiting S14 expression may have the same effect as pharmacologic inhibition of FAS and would therefore make S14 an excellent target for anti-neoplastic therapies.
Publisher
ProQuest Dissertations & Theses
Subject
ISBN
9780599455665, 0599455667
