Alterations of Inflammatory Mediators (TNF-α and HMGB1) and Circulating microRNA-22 Expression in Pre- and...

Ovarian cancer is an important cause of cancer-related mortality among women, disease severity increases due to hormonal changes, which modify the ovarian environment and may contribute to the development of ovarian cancer (OC). Inflammatory mediators play a central role in the enhancement of OC progression. Several microRNA play central role in OC; microRNA-22 (miR-22) is a biomarker associated with hormonal status regarding menopause and the development of ovarian cancer. Evaluating these biomarkers and assess the interaction among them, may contribute to a deeper understanding of the disease mechanism and can improve diagnostic accuracy.

Assess CA125, TNF-α, HMGB1, and miR-22 levels in pre- and post-menopausal epithelial ovarian cancer (EOC) patients as well as the correlation of these factors and their impact on EOC progression in pre- and post- menopausal patients.

120 women enrolled in this study were divided into four groups (n=30 for each group): two control groups (healthy premenopausal and postmenopausal) and two patient groups (premenopausal and postmenopausal with EOC). Serum levels of CA125, TNF-α, HMGB, and miR-22 expression were measured. Statistical analysis was performed to compare groups and to assess correlations within patient groups at (p< 0.05) using SPSS Statistics analysis version 26.

All biomarkers showed statistically significant differences among groups at p < 0.05. levels of CA125, HMGB1, and TNF-α were significantly increased in EOC groups Especially in the postmenopausal group. Expression of serum miR-22 was significantly decreased in EOC patient groups compared to control groups. Regarding correlation analyses, there were positive associations between TNF-α and HMGB1 in patient groups. Conversely, the expression of miRN-22 was inversely correlated with HMGB1.

The relative expression level of miR-22 significantly decreases depending on menopausal and inflammatory status, suggesting that miR-22 plays as tumor suppressor role and is negatively affected by inflammation.