Follicular stimulating hormone enhances Notch 1 expression in SK-OV-3 ovarian cancer cells / 부인종양
Journal of Gynecologic Oncology
;
: 119-124, 2010.
Article
in English
| WPRIM
| ID: wpr-60976
ABSTRACT
OBJECTIVE:
Notch is known as a transmembranous receptor family with four homologous forms - Notch 1, Notch 2, Notch 3, and Notch 4 and related to cell fate regulation and angiogenesis. The purpose is to investigate the effect of follicular stimulating hormone (FSH) on the Notch 1 expression and proliferation in ovarian cancer cells.METHODS:
Human ovarian cancer cell line, SK-OV-3 and FSH were used. XTT cell proliferation and cell migration assay were carried out with FSH 100 mIU/mL and Notch 1 siRNA. Western blots and reverse transcriptase-polymerase chain reactions (RT-PCR) were carried out to determine the expression level of the Notch 1 protein and mRNA with FSH treatment in 0, 1, 5, 10, 100, 200, 300 mIU/mL concentrations. Immunofluorescent (IF) stains were performed in SK-OV-3 cell cultures with FSH 100 mIU/mL. Student-t tests were used in statistical analyses.RESULTS:
The SK-OV-3 have Notch 1 receptors in their natural status. FSH stimulated SK-OV-3 cells in XTT cell proliferation and cell migration assays and notch 1 siRNA inhibited. The expression level of Notch 1 protein and mRNA were increased in a dose dependent pattern according to FSH concentrations compared to untreated cells. IF stains also showed brighter Notch1 expressions in the FSH treated cells compared to the control cells.CONCLUSION:
FSH enhances proliferation & migration and Notch 1 signaling in SK-OV-3 cells. The Notch signaling probably supports one of the cell proliferating mechanisms of FSH in ovarian cancer cells.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Ovarian Neoplasms
/
RNA, Messenger
/
Cell Line
/
Blotting, Western
/
Cell Culture Techniques
/
RNA, Small Interfering
/
Cell Proliferation
/
Coloring Agents
/
Cell Migration Assays
Limits:
Humans
Language:
English
Journal:
Journal of Gynecologic Oncology
Year:
2010
Type:
Article
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