Aberrant STYK1 expression in ovarian cancer tissues and cell lines

• Main Authors: Jackson Kesmic A (Author), Oprea Gabriela (Author), Handy Jeffrey (Author), Kimbro K Sean (Author)
• Format: Book
• Published: BMC, 2009-10-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.

Summary

<p>Abstract</p> <p>Background</p> <p>Overexpression of <it>STYK1</it>, 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 <it>in vivo</it>, collectively, suggesting an oncogenic role for STYK1.</p> <p>Methods</p> <p>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.</p> <p>Results</p> <p>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 <it>STYK1 </it>as determined by RT-PCR. Estradiol treatment of these cells resulted in up- and down-regulation of <it>STYK1 </it>despite estrogen receptor status; whereas G-1, a GPR30-specific agonist, increased STYK1 mRNA levels higher than that of estradiol.</p> <p>Conclusion</p> <p>We conclude that <it>STYK1 </it>is expressed in ovarian cancer and is regulated by estrogen through a GPR30 hormone-signaling pathway, to the exclusion of estrogen receptor-alpha.</p>

Item Description

10.1186/1757-2215-2-15
1757-2215