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Published on: November 2, 2014
Aberrant STYK1 expression in ovarian cancer tissues and cell lines
Kesmic A Jackson1, Gabriela Oprea, Jeffrey Handy
1Department of Hematology and Medical Oncology, Winship Cancer Institute, Emory University School of Medicine, Building C, Room C4090, Atlanta, GA 30322, USA. kskimbr@emory.edu.
Background:
Overexpression of STYK1, a putative serine/threonine and tyrosine receptor protein kinase has been shown to confer tumorigenicity and metastatic potential to normal cells injected into nude mice. Mutation of a tyrosine residue in the catalytic STYK1 domain attenuates the tumorigenic potential of tumor cells in vivo, collectively, suggesting an oncogenic role for STYK1.
Methods:
To investigate the role of STYK1 expression in ovarian cancer, a panel of normal, benign, and ovarian cancer tissues was evaluated for STYK1 immunoreactivity using STYK1 antibodies. In addition, mRNA levels were measured by reverse transcription PCR and real-time PCR of estrogen receptors, GPR30 and STYK1 following treatment of ovarian cell lines with estrogen or G1, a GPR30 agonist, as well as western analysis.
Results:
Our data showed higher expression of STYK1 in cancer tissues versus normal or benign. Only normal or benign, and one cancer tissue were STYK1-negative. Moreover, benign and ovarian cancer cell lines expressed STYK1 as determined by RT-PCR. Estradiol treatment of these cells resulted in up- and down-regulation of STYK1 despite estrogen receptor status; whereas G-1, a GPR30-specific agonist, increased STYK1 mRNA levels higher than that of estradiol.
Conclusion:
We conclude that STYK1 is expressed in ovarian cancer and is regulated by estrogen through a GPR30 hormone-signaling pathway, to the exclusion of estrogen receptor-alpha.
Insights
STYK1 (serine/threonine and tyrosine receptor protein kinase) is overexpressed in ovarian cancer. Estrogen, via GPR30, regulates STYK1, suggesting a role in ovarian tumorigenesis.
Area of Science:
- Oncology
- Molecular Biology
- Endocrinology
Background:
- STYK1 (serine/threonine and tyrosine receptor protein kinase) overexpression confers tumorigenicity and metastatic potential.
- STYK1's oncogenic role is suggested by its ability to promote tumor cell growth and metastasis.
- STYK1's role in ovarian cancer warrants investigation due to its association with tumorigenesis.
Purpose of the Study:
- To investigate the expression of STYK1 in ovarian cancer tissues and cell lines.
- To determine the regulatory role of estrogen and GPR30 in STYK1 expression in ovarian cancer.
Main Methods:
- Immunohistochemical analysis of STYK1 in normal, benign, and ovarian cancer tissues.
- Reverse transcription PCR and real-time PCR to measure STYK1, estrogen receptors, and GPR30 mRNA levels.
- Western blot analysis to assess protein expression following treatment with estradiol or G1 (GPR30 agonist).
Main Results:
- STYK1 expression was significantly higher in ovarian cancer tissues compared to normal or benign tissues.
- Ovarian cancer and benign cell lines expressed STYK1 mRNA.
- Estradiol and G1 treatment modulated STYK1 mRNA levels, with G1 showing a more pronounced effect.
Conclusions:
- STYK1 is expressed in ovarian cancer.
- Estrogen regulates STYK1 expression in ovarian cancer through the GPR30 signaling pathway.
- Estrogen receptor-alpha is not involved in the regulation of STYK1 by estrogen in ovarian cancer.
