MicroRNA-326 as a Tumor Suppressor Regulates the NOB1 Expression in Breast Cancer

Aberrant expression of miR-326, a microRNA involved in tumor suppression, has been associated with a broad range of diseases, including cancer and autoimmune disorders. The NOB1 gene (NIN One Binding Protein 1 Homolog) is a critical component that plays a pivotal role in the biogenesis and proper functioning of the 26S proteasome. Researchers have found that miR-326 acts as a regulator of NOB1 expression by targeting its mRNA, ultimately leading to a decrease in NOB1 protein translation.

This study seeks to assess the expression levels of miR-326 and NOB1 genes within breast cancer (BC) tumor tissue, along with an examination of their potential correlation, in comparison to both normal-adjacent (NATs) and healthy tissues. Forty-one BC, NATs, and eight healthy breast tissues were used. To compare the expression profiles of miR-326 and NOB1 in different tissue groups, including BC, NATs, and healthy tissues, quantitative real-time PCR (qRT-PCR) was used.

miR-326 expression was significantly decreased in BC tissues compared with NATs (p < 0.0001) and healthy tissues (p < 0.0001). The expression levels of NOB1 were increased significantly in BC tissue compared with NATs (p < 0.0001) and healthy tissues (p < 0.0001). A significant negative correlation was observed between miR-326 and NOB1 expression (p < 0.005). Receiver-operating characteristic (ROC) curve analysis showed that AUC = 0.8349 and AUC = 0.7 are for miR-326 and NOB1, respectively.

Decreasing the expression of miR-326 in patients with BC may affect its target gene (NOB1) and probably lead to an increase in the expression of the NOB1 gene. This negative correlation suggests a potential regulatory role for miR-326 in controlling NOB1 expression. Our findings demonstrate that dysregulation of the miR-326 and NOB1 expression levels may contribute to BC development and progression, indicating the potential of these two genes as biomarkers for diagnostic and therapeutic approaches in BC.