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A study of the effect of an anti-pro...

Chacko, Sapna Mani.

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A study of the effect of an anti-proliferative agent on rat glial tumor cells: Effects on insulin-like growth factor-1 gene expression and action.

Record Type:	Language materials, printed : Monograph/item
Title/Author:	A study of the effect of an anti-proliferative agent on rat glial tumor cells: Effects on insulin-like growth factor-1 gene expression and action./
Author:	Chacko, Sapna Mani.
Description:	200 p.
Notes:	Adviser: Martin Adamo.
Contained By:	Dissertation Abstracts International62-12B.
Subject:	Chemistry, Biochemistry. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3037924
ISBN:	0493515151

A study of the effect of an anti-proliferative agent on rat glial tumor cells: Effects on insulin-like growth factor-1 gene expression and action.
Chacko, Sapna Mani.

A study of the effect of an anti-proliferative agent on rat glial tumor cells: Effects on insulin-like growth factor-1 gene expression and action. - 200 p.

Adviser: Martin Adamo.

Thesis (Ph.D.)--The University of Texas Health Science Center at San Antonio, 2002.

Poly (IC), a synthetic double-stranded RNA co-polymer of inosinic and cytidilic acids, decreases proliferation of normal and tumorigenic cells. I tested the hypothesis that Poly (IC) decreased proliferation of C6 rat glioma cells by disrupting an autocrine IGF-1 growth loop. Poly (IC) decreased the numbers of confluent and sub-confluent C6 cultures. Addition of IGF-1 partially blocked the Poly (IC)-mediated decrease in C6 cell number, suggesting that one mechanism of Poly (IC) action is through down-regulation of IGF-1 gene expression and/or action.

ISBN: 0493515151Subjects--Topical Terms:

1017722
Chemistry, Biochemistry.

A study of the effect of an anti-proliferative agent on rat glial tumor cells: Effects on insulin-like growth factor-1 gene expression and action.
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040 $a UnM $c UnM
100 1 $a Chacko, Sapna Mani. $3 1259011
245 1 0 $a A study of the effect of an anti-proliferative agent on rat glial tumor cells: Effects on insulin-like growth factor-1 gene expression and action.
300 $a 200 p.
500 $a Adviser: Martin Adamo.
500 $a Source: Dissertation Abstracts International, Volume: 62-12, Section: B, page: 5700.
502 $a Thesis (Ph.D.)--The University of Texas Health Science Center at San Antonio, 2002.
520 $a Poly (IC), a synthetic double-stranded RNA co-polymer of inosinic and cytidilic acids, decreases proliferation of normal and tumorigenic cells. I tested the hypothesis that Poly (IC) decreased proliferation of C6 rat glioma cells by disrupting an autocrine IGF-1 growth loop. Poly (IC) decreased the numbers of confluent and sub-confluent C6 cultures. Addition of IGF-1 partially blocked the Poly (IC)-mediated decrease in C6 cell number, suggesting that one mechanism of Poly (IC) action is through down-regulation of IGF-1 gene expression and/or action.
520 $a Poly (IC) decreased IGF-1, IGF-1 receptor, IGFBP-4 and IGFBP-5 mRNA levels and decreased immunoreactive IGF-1 peptide, and IGF-1 receptor βIGFBP-3, IGFBP-4, and IGFBP-5 protein levels in C6 cells. Poly (IC) decreased IGF-1 mRNA independent of new protein synthesis in general and type I interferon (IFN) synthesis in particular. Poly (IC) decreased IGF-1 gene transcription, but did not alter IGF-1 mRNA stability. Poly (IC) activated protein kinase R (PKR) at 5 minutes and increased PKR protein levels at 48 and 72 hours. IGF-1 did not prevent Poly (IC) from activating PKR, but inhibited Poly (IC) from increasing PKR protein levels.
520 $a Poly (IC) caused a block in G1 to S transition in confluent C6 cultures whereas in sub-confluent cultures, Poly (IC) decreased the percentage of cells in the G2/M phase. Addition of IGF-1 to Poly (IC)-treated cells decreased the percentage of cells in G0/G1 phase and increased the percentage of cells in G2/M phase in confluent and sub-confluent C6 cultures, indicating reversal of cell cycle blocks. Inhibiting PKR activation also partially prevented the Poly (IC)-mediated cytostasis of C6 cells. Both IGF-1 and a blocking antibody against IFN prevented the increase of PKR levels and the decreased cell proliferation caused by Poly (IC). I conclude that Poly (IC) induces IFN, which mediates the cytostatic effect of Poly (IC) on C6 cells, at least in part through PKR. IGF-1 prevents IFN from inducing PKR, thus explaining the ability of IGF-1 to reverse the cell cycle blocks and the decreased C6 proliferation caused by Poly (IC).
590 $a School code: 0853.
650 4 $a Chemistry, Biochemistry. $3 1017722
650 4 $a Health Sciences, Oncology. $3 1018566
690 $a 0487
690 $a 0992
710 2 0 $a The University of Texas Health Science Center at San Antonio. $3 1030926
773 0 $t Dissertation Abstracts International $g 62-12B.
790 $a 0853
790 1 0 $a Adamo, Martin, $e advisor
791 $a Ph.D.
792 $a 2002
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3037924