MicroRNA-326 as a Tumor Suppressor Regulates the NOB1 Expression in Breast Cancer
TL;DR
It is demonstrated 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.
Abstract
Background 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. Methods 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. Results 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. Conclusion 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.