The present study has focused on the identification of the differences between expression patterns of kinin-dependent genes in endometrial cancer with the use of real-time quantitative reverse transcription polymerase chain reaction and oligonucleotide microarray.
The study group consisted of 50 endometrium samples collected from women with endometrial cancer. Gene expression of kinin receptors BR1 and BR2 was evaluated with real-time quantitative reverse transcription polymerase chain reaction. The analysis of the expression profile of genes related to the kinin mitogenic signal transduction pathway was performed using HG-U133A oligonucleotide microarrays.
The transcriptional activity of the B1 receptor for kinins increased in patients with grade 1 (G1) and grade 2 (G2) endometrial cancer when compared to the control group, whereas it decreased in patients with grade 3 (G3) endometrial cancer. The expression of the B2 receptor showed a growing trend reaching the peak in the G2, whereas G3 was characterized by a decrease in the gene transcriptional activity. Significant differential gene expression was recorded for GNB1, PRKAR1A, KRAS, MAP2K2, GNG5, MAPK1, ADCY9, GNG11, JUN, PRKCA, PRKACB, FOS, PLCB4, ADCY8, and GNG12.
The expression changes in kinin-dependent genes might cause disturbance in the underlying biological processes, which could be important for the pathogenesis of endometrial cancer. This will eventually help to improve treatment strategies for patients with endometrial cancer in the future.
*Department of Molecular Biology, Medical University of Silesia, Sosnowiec; and †Department of Gynecology, Obstetrics, and Oncologic Gynecology, Medical University of Silesia, Bytom, Poland.
Address correspondence and reprint requests to Malgorzata Kimsa, PhD, Department of Molecular Biology, Medical University of Silesia, Narcyzow 1, 41-200 Sosnowiec, Poland. E-mail: firstname.lastname@example.org.
This work was supported by grant number KNW-2-003/09.
The authors declare that there are no conflicts of interest.
Received February 1, 2012
Accepted April 11, 2012