Tahtasakal Reyhan, Hamurcu Zuhal, Oz Abdullah Bahadir, Balli Mustafa, Dana Halime, Gok Mustafa, Cinar Venhar, Inanc Mevlude, Sener Elif Funda
Erciyes University Genome and Stem Cell Center (GENKOK), Kayseri, Türkiye.
Department of Medical Biology, Erciyes University Medical Faculty, Kayseri, Türkiye.
Ann Surg Oncol. 2025 Apr;32(4):2994-3008. doi: 10.1245/s10434-024-16656-0. Epub 2024 Dec 18.
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.
This study aimed to determine the change in miR-484 in different BC cells and its relationship with the apoptosis pathway.
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.
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.
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.
乳腺癌（BC）是女性最常见的死亡原因之一。癌细胞逃避凋亡，导致细胞不受控制地增殖。已知微小RNA（miRNA）可调节癌细胞中的凋亡。
本研究旨在确定不同BC细胞中miR-484的变化及其与凋亡途径的关系。
在本研究中，从42例患者（6例良性，36例恶性）中收集肿瘤及肿瘤旁的健康组织样本。组织样本根据肿瘤类型、肿瘤组织学分级、增殖指数和分子亚型进行分类。通过定量实时聚合酶链反应（qRT-PCR）测定基因表达水平，使用蛋白质印迹法测定蛋白质水平。结果采用ΔΔCt法进行分析。
研究结果表明，miR-484在恶性肿瘤中的表达水平高于良性肿瘤，在肿瘤组织中的表达水平高于健康组织。此外，还确定随着Ki-67水平、组织学分级和侵袭性的增加，miR-484的表达水平也增加。与相邻健康组织相比，肿瘤组织中BCL2表达增加，Casp3和Casp9表达减少。因此，发现miR-484表达与BCL2之间呈正相关，CASP3和CASP9表达之间呈负相关。
我们的结果表明，miR-484在BC中可能作为一种癌基因miRNA发挥作用。乳腺肿瘤组织中miR-484和BCL2增加，Casp3减少表明，Casp9表达可能通过抑制BC细胞凋亡增加细胞不受控制的增殖，并可能促进肿瘤进展。
