No abstract

Ovarian cancer is one of the most commonly occurring types of cancer and one of the most common causes of cancer-associated mortality in women. Diagnosis of ovarian cancer at an early stage is difficult due to the lack of specific symptoms. In the present study, it is demonstrated that active vitamin D treatment prohibited the proliferation and invasion of ovarian cancer cells, and the expression level of a germ cell specific marker DEAD (Asp-Glu-Ala-Asp)-box helicase 4 (DDX4), which is overexpressed in ovarian cancer, was downregulated by active vitamin D treatment. Knockdown of DDX4 by siRNA could also suppress the invasive ability of ovarian cancer cells. Therefore, DDX4 may be considered as a diagnostic marker of ovarian cancer, and vitamin D may be a candidate drug for ovarian cancer therapy.

BackgroundMicroRNAs (miRNAs) are a class of small non-coding RNAs, which post-transcriptionally repress the expression of genes involved in cancer initiation and progression. Although some miRNAs that target many signaling pathways (also called universe miRNAs) are supposed to play a global role in diverse human tumors, their regulatory functions in gynecological cancers remain largely unknown. We investigated the biological role and underlying mechanism of miR-548c (one universe miRNA) in endometrial and ovarian cancer.MethodsThe effects of miR-548c overexpression on cell proliferation, migration and invasion were studied in endometrial and ovarian cancer cells. TWIST1 (Twist) was identified as a direct miR-548c target by western blot analysis and luciferase activity assay. The expression of miR-548c and Twist were examined by qRT-PCR in endometrial and ovarian cancer tissues.ResultsHere, we report that miR-548c is down-regulated in endometrial and ovarian cancer tissues when compared to normal tissues, and our meta-analysis reveal that decreased miR-548c expression correlates with poor prognosis in endometrial cancer patients. We show that in endometrial and ovarian cancer cells, ectopic expression of miR-548c significantly inhibits whereas knockdown of miR-548c dramatically induces cancer cell proliferation, migration and invasion. By using luciferase reporter assay, we demonstrate that Twist, a known oncogene in endometrial and ovarian cancers, is a direct target of miR-548c. Furthermore, the expression of Twist partially abrogates the tumor suppressive effects of miR-548c on cell migration and invasion.ConclusionThese findings suggest that miR-548c directly downregulates Twist, and provide a novel mechanism for Twist upregulation in both endometrial and ovarian cancers. The use of miR-548c may hold therapeutic potential for the treatment of Twist-overexpressing tumors.