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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.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	A novel role for JAK/STAT signaling in cell migration during development and in cancer./
作者:	Silver, Debra Lynn.
面頁冊數:	177 p.
附註:	Source: Dissertation Abstracts International, Volume: 64-02, Section: B, page: 0529.
Contained By:	Dissertation Abstracts International64-02B.
標題:	Biology, Genetics. -
電子資源:	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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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.
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650 4 $a Biology, Cell. $3 1017686
650 4 $a Health Sciences, Oncology. $3 1018566
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710 2 0 $a The Johns Hopkins University. $3 1017431
773 0 $t Dissertation Abstracts International $g 64-02B.
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791 $a Ph.D.
792 $a 2003
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