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A novel role for JAK/STAT signaling ...

Silver, Debra Lynn.

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A novel role for JAK/STAT signaling in cell migration during development and in cancer.

Record Type:	Electronic resources : Monograph/item
Title/Author:	A novel role for JAK/STAT signaling in cell migration during development and in cancer./
Author:	Silver, Debra Lynn.
Description:	177 p.
Notes:	Source: Dissertation Abstracts International, Volume: 64-02, Section: B, page: 0529.
Contained By:	Dissertation Abstracts International64-02B.
Subject:	Biology, Genetics. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3080766

A novel role for JAK/STAT signaling in cell migration during development and in cancer.
Silver, Debra Lynn.

A novel role for JAK/STAT signaling in cell migration during development and in cancer. - 177 p.

Source: Dissertation Abstracts International, Volume: 64-02, Section: B, page: 0529.

Thesis (Ph.D.)--The Johns Hopkins University, 2003.

The JAK/STAT signaling pathway is essential for the proliferation, survival, and growth of many cells including cancer cells. We have found a novel in vivo function for this signaling pathway in cell migration in the Drosophila ovary and in ovarian cancer cells.Subjects--Topical Terms:

1017730
Biology, Genetics.

A novel role for JAK/STAT signaling in cell migration during development and in cancer.
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035 $a (UnM)AAI3080766
035 $a AAI3080766
040 $a UnM $c UnM
100 1 $a Silver, Debra Lynn. $3 1949450
245 1 2 $a A novel role for JAK/STAT signaling in cell migration during development and in cancer.
300 $a 177 p.
500 $a Source: Dissertation Abstracts International, Volume: 64-02, Section: B, page: 0529.
500 $a Adviser: Denise J. Montell.
502 $a Thesis (Ph.D.)--The Johns Hopkins University, 2003.
520 $a The JAK/STAT signaling pathway is essential for the proliferation, survival, and growth of many cells including cancer cells. We have found a novel in vivo function for this signaling pathway in cell migration in the Drosophila ovary and in ovarian cancer cells.
520 $a A requirement for STAT in border cell migration was revealed from an EMS screen for mutants that show defective border cell migration in mosaic clones. In the Drosophila ovary, 6--10 epithelial cells are recruited to a cluster and migrate together over a six hour period. The ligand for this pathway, unpaired, is expressed by two central cells of the cluster and is required in these cells for the recruitment of the outer border cells and their subsequent migration. Loss of jak, stat or the receptor, called domeless, each of which is expressed by the outer border cells, inhibits border cell migration and the normal recruitment of border cells to the cluster. Furthermore, ectopic expression of JAK or UPD is sufficient to induce extra epithelial cells to become migratory.
520 $a We were interested in extending our observations to the study of ovarian cancer cells. STAT3 is constitutively activated in many human cancers, including ovarian cancer, which is derived from epithelial cells. We have found that activated STAT3 is localized to both nuclei and focal adhesions of ovarian cancer cells and can be found in a protein complex with focal adhesion proteins. Inhibition of STAT3 in SKOV3 cells, either pharmacologically or by siRNA, inhibits cell migration in a boyden chamber assay. These results suggest that inhibiting JAK/STAT signaling in cancer, might not only shrink the tumor, but could reduce its metastatic potential as well.
590 $a School code: 0098.
650 4 $a Biology, Genetics. $3 1017730
650 4 $a Biology, Cell. $3 1017686
650 4 $a Health Sciences, Oncology. $3 1018566
690 $a 0369
690 $a 0379
690 $a 0992
710 2 0 $a The Johns Hopkins University. $3 1017431
773 0 $t Dissertation Abstracts International $g 64-02B.
790 1 0 $a Montell, Denise J., $e advisor
790 $a 0098
791 $a Ph.D.
792 $a 2003
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3080766