Master of Science / Department of Animal Sciences and Industry / Timothy G. Rozell / Follicle stimulating hormone (FSH) is known as the key hormone capable of
causing proliferation of granulosa cells in the ovary. The classical receptor belongs to the
G protein-coupled superfamily and is designated FSHR-1. A variant in the FSH receptor
has been shown to be functional in mouse ovaries. The variant receptor is designated as
FSHR-3, and when bound by FSH activates a pathway that shares similar characteristics
to the growth factor type I receptor pathway, with no increase in cAMP. The FSHR-3
variant activates MAPK upon binding to FSH, and causes proliferation of cells on which
it is known to be expressed. For example ID8 mouse ovarian surface epithelium cells
(MOSEC), a cell line that when introduced in immunocompetent mice causes tumors
similar to human ovarian cancer and which also express FSHR-3, proliferated in response
to FSH. The present study explored the potential for decreasing expression of FSHR-3
protein. The RNA interference (RNAi) technique was used to insert small inhibitory
RNA(siRNA) segments corresponding specifically to the R3 variant of the FSH receptor
in ID8 MOSEC. Transfected cells were lysed and FSHR-3 protein was visualized using
SDS Page and Western blotting analysis. A reduction in expression of FSHR-3 was
observed in two of the transfection groups, with the greatest down-regulation of FSHR-3
being 30.1%. From these preliminary results we conclude that the FSHR-3 is expressed
on ID8 cells, and that siRNA may be useful to reduce its expression. Thus, it may be
possible to slow the growth of FSH-responsive tumors using siRNA to target the FSHR-3 receptor.
| Identifer | oai:union.ndltd.org:KSU/oai:krex.k-state.edu:2097/495 |
| Date | January 1900 |
| Creators | Zimmerman, Shawn |
| Publisher | Kansas State University |
| Source Sets | K-State Research Exchange |
| Language | en_US |
| Detected Language | English |
| Type | Thesis |
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