Project Details
Abstract
Ovarian cancer is the leading cause of gynecological cancer death. The high
case-fatality rate is mainly attributed to the fact that most ovarian cancers are
undiagnosed until advanced stages, III or IV, where the cancer has spread beyond the
pelvis. More tumor markers for early detection of ovarian cancer are thus warranted.
Through a systematic proteomics search for biomarkers of ovarian cancer, we have
identified stress-induced phosphoprotein-1 (STIP1) as a potential biomarker for
ovarian cancer. Because of the presence of STIP1 in various types of cancers, we
hypothesize that STIP1 may have anti-apoptotic and/or pro-growth nature. Based on
our discovery that STIP1 is secreted from tumors, we hypothesize that STIP1 may be
a means by which the cancer gains survival advantages by stimulating itself (autocrine)
and remodeling its environment (paracrine). Since there are nuclear localization signal
(NLS) and several phosphorylating sites in STIP1 protein, we speculate that a panel of
kinases and phosphatases may regulate translocation of STIP1, which in turns exerts
diverse functions. In this three-year project, we attempt to achieve four Specific Aims:
(1) to delineate the changes in serum STIP1 levels during menstruation cycle and to
test whether polymorphisms of STIP1 are associated with ovarian cancer, (2) to
identify the functions of upregulated intracellular STIP1 in ovarian cancer cells, (3) to
study how STIP1 is secreted from ovarian cancer cells, and (4) to elucidate how
secreted STIP1 exerts action in an autocrine or paracrine fashion. After we have
completed this three-year study, we will fill the current knowledge gaps about the role
of STIP1 in tumor biology. Our further understanding of STIP1 may provide the
foundation for future development of novel therapeutic strategies for human ovarian
cancer by targeting STIP1.
Project IDs
Project ID:PC10101-2042
External Project ID:NSC100-2314-B182-016-MY3
External Project ID:NSC100-2314-B182-016-MY3
Status | Finished |
---|---|
Effective start/end date | 01/08/12 → 31/07/13 |
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