Introduction/Background Ovarian cancer (OC) is the most common cause of gynecological cancer-related death in developed countries. The absence of evident early symptoms and effective asymptomatic population screening leads to diagnosis in advanced stages for the majority of patients and, thus, to poor prognosis. Consequently, the identification of predictive markers of patients´ treatment outcome could ameliorate disease management. microRNA-34a (miR-34a) is highlighted to exert a tumor suppressive role in several malignancies and is downregulated in numerous cancers. According to TarBase v.8, highthroughput studies have reported the negative correlation of miR-34a with kallikrein-related peptidase 6 (KLK6) expression levels. In the present study, we aimed to investigate the expression profile of miR-34a in ovarian carcinomas and to explore its clinical value in OC patients.

Methodology Ovarian cancer specimens and matched adjacent tissues were obtained from St. Savvas Regional Anticancer Oncology Hospital of Athens. Following homogenization, total RNA was extracted using TRI reagent. Thereafter, the RNA was polyadenylated in the 3’-end and first-strand cDNA synthesis was performed by MMLV using an oligo (dT) adapter. A SYBR-Green fluorescent-based qPCR assay was developed to quantify miR-34a, using snoRNA RNU48 as endogenous reference control gene for normalization purposes. Extensive statistical analysis has been conducted to explore the clinical utility of miR-34a levels.

Results The expression analysis demonstrated that miR-34a levels are downregulated in ovarian tumors compared to normal epithelium. With regard to clinicopathological characteristics, patients with tumor grade 3 (G3) were highlighted to underexpress miR-34a compared to OC patients with tumor grade 1 (G1) or 2 (G2). Ultimately, no association was observed between FIGO stages and miR-34a expression levels.

Conclusion The tumor-suppressor miR-34a is downregulated in ovarian malignant epithelium and correlated with higher tumor grading, supporting its further evaluation as a potential molecular marker in OC prognosis.

Disclosure Nothing to disclose