miR-484 as an "OncomiR" in Breast Cancer Promotes Tumorigenesis by Suppressing Apoptosis Genes.

Purpose: Breast cancer (BC) is one of the most common causes of death among females. Cancer cells escape from apoptosis, causing the cells to proliferate uncontrollably. MicroRNAs (miRNAs) are known to regulate apoptosis in cancer cells.

Objective: This study aimed to determine the change in miR-484 in different BC cells and its relationship with the apoptosis pathway.

Methods: In the study, tumor and healthy tissue samples adjacent to the tumor were collected from 42 patients (6 benign, 36 malignant). Tissue samples were classified according to tumor type, tumor histological grade, proliferation index, and molecular subtypes. Gene expression levels were determined by quantitative real-time polymerase chain reaction (qRT-PCR), and protein levels were determined using the Western Blot method. The results were analyzed using the delta-delta Ct method.

Results: Findings showed that miR-484 expression levels were higher in malignant tumors than in benign tumors, and higher in tumor tissues than healthy tissues. Additionally, it was determined that as Ki-67 levels and histological grade and aggressiveness increased, miR-484 expression levels also increased. In tumor tissue compared with healthy adjacent tissue, there was an increase in BCL2 expression and a decrease in Casp3 and Casp9 expression. Therefore, a positive correlation was found between miR-484 expression and BCL2, and a negative correlation was found between CASP3 and CASP9 expression.

Conclusion: Our results show that miR-484 may play a roll as an onco-miR in BC. Increased miR-484 and BCL2, and decreased Casp3, in breast tumor tissues suggest that Casp9 expression may increase uncontrolled cell proliferation by suppressing apoptosis in BC cells and may contribute to tumor progression.