Breast cancer is a disease characterized by progressive genetic abnormalities including mutations in tumor suppressor genes and oncogenes, as well as other chromosomal abnormalities. Protein inhibitor of activated signal transducer and activator of transcription 3 (PIAS3) is a member of the PIAS family of transcriptional modulators; its expression is altered in many cancers. Micro-ribonucleic acid (miRNA)-18a acts as an oncogene by negatively regulating PIAS3 and thus modulating the expression of signal transducer and activator of transcription 3 (STAT3) target genes. The aim of this work is to examine the expression levels of PIAS3 gene and miRNA-18a in breast cancer tissues and nearby non-tumor tissues. The samples of breast cancer and paired samples of non-cancerous tissue from the same resected breast were obtained from 25 patients undergoing surgery. Full history taking, complete physical examination, pre-operative fine-needle aspiration cytology or ultrasonic (U/S)-guided core biopsy from the breast mass, final surgical biopsy for pathological examination, and routine laboratory investigations were done. Estrogen receptors (ER), progesterone receptors (PR), and human epidermal growth factor receptor 2 (HER2) status were evaluated. Total RNA extraction followed by real-time reverse transcription-polymerase chain reaction (RT-PCR) for quantification of PIAS3 mRNA and miRNA-18a expressions was performed. The mean value of PIAS3 mRNA fold expression was significantly lower in the tumor group (5.12 ± 9.85) compared to the normal group (8.38 ± 17.10) (p = 0.040). miRNA-18a fold expression was higher among tumor group (3.5 ± 7.4) than that of normal group (2.5 ± 3), however, it did not reach the level of statistical significance (p = 0.861). miRNA-18a fold expression had negative significant correlation with PIAS3 mRNA fold expression (p = 0.018). A significant association was observed between miRNA-18a expression in breast cancer tissues and the pathological grade of the tumor (p = 0.029). The results of this study showed that PIAS3 mRNA and miRNA-18a might be of importance in breast cancer development and pathogenesis, and this may be reflected on the treatment strategies targeting STAT3 pathway. However, further studies with larger sample size are needed to validate these observations.

中文翻译：

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活化STAT3和miRNA-18a表达蛋白抑制剂在乳腺癌中的作用

乳腺癌是一种以进行性遗传异常为特征的疾病，包括抑癌基因和癌基因的突变，以及其他染色体异常。激活信号转导蛋白抑制剂和转录激活因子 3 (PIAS3) 是 PIAS 转录调节剂家族的成员；它的表达在许多癌症中发生了改变。微核糖核酸 (miRNA)-18a 作为致癌基因通过负调节 PIAS3 从而调节信号转导和转录激活因子 3 (STAT3) 靶基因的表达。这项工作的目的是检查 PIAS3 基因和 miRNA-18a 在乳腺癌组织和附近非肿瘤组织中的表达水平。从接受手术的25名患者中获得乳腺癌样本和来自同一切除乳房的非癌组织的配对样本。完成了完整的病史采集、完整的体格检查、术前细针抽吸细胞学或超声 (U/S) 引导下的乳房肿块核心活检、病理检查的最终手术活检和常规实验室检查。评估了雌激素受体 (ER)、孕激素受体 (PR) 和人类表皮生长因子受体 2 (HER2) 的状态。进行总 RNA 提取，然后进行实时逆转录聚合酶链反应 (RT-PCR) 以定量 PIAS3 mRNA 和 miRNA-18a 表达。与正常组（8.38±17）相比，肿瘤组PIAS3 mRNA倍数表达的平均值（5.12±9.85）显着降低。10) (p = 0.040)。肿瘤组中miRNA-18a倍数表达（3.5±7.4）高于正常组（2.5±3），但未达到统计学显着性水平（p=0.861）。miRNA-18a 倍数表达与 PIAS3 mRNA 倍数表达呈显着负相关（p = 0.018）。在乳腺癌组织中观察到 miRNA-18a 表达与肿瘤病理分级之间存在显着关联（p = 0.029）。本研究结果表明 PIAS3 mRNA 和 miRNA-18a 可能在乳腺癌的发生发展和发病机制中起重要作用，这可能反映在靶向 STAT3 通路的治疗策略上。然而，需要更大样本量的进一步研究来验证这些观察结果。4）比正常组（2.5±3），但没有达到统计学显着性水平（p=0.861）。miRNA-18a 倍数表达与 PIAS3 mRNA 倍数表达呈显着负相关（p = 0.018）。在乳腺癌组织中观察到 miRNA-18a 表达与肿瘤病理分级之间存在显着关联（p = 0.029）。本研究结果表明 PIAS3 mRNA 和 miRNA-18a 可能在乳腺癌的发生发展和发病机制中起重要作用，这可能反映在靶向 STAT3 通路的治疗策略上。然而，需要更大样本量的进一步研究来验证这些观察结果。4）比正常组（2.5±3），但没有达到统计学显着性水平（p = 0.861）。miRNA-18a 倍数表达与 PIAS3 mRNA 倍数表达呈显着负相关（p = 0.018）。在乳腺癌组织中观察到 miRNA-18a 表达与肿瘤病理分级之间存在显着关联（p = 0.029）。本研究结果表明 PIAS3 mRNA 和 miRNA-18a 可能在乳腺癌的发展和发病机制中具有重要意义，这可能反映在针对 STAT3 通路的治疗策略上。然而，需要更大样本量的进一步研究来验证这些观察结果。miRNA-18a 倍数表达与 PIAS3 mRNA 倍数表达呈显着负相关（p = 0.018）。在乳腺癌组织中观察到 miRNA-18a 表达与肿瘤病理分级之间存在显着关联（p = 0.029）。本研究结果表明 PIAS3 mRNA 和 miRNA-18a 可能在乳腺癌的发生发展和发病机制中起重要作用，这可能反映在靶向 STAT3 通路的治疗策略上。然而，需要更大样本量的进一步研究来验证这些观察结果。miRNA-18a 倍数表达与 PIAS3 mRNA 倍数表达呈显着负相关（p = 0.018）。在乳腺癌组织中观察到 miRNA-18a 表达与肿瘤病理分级之间存在显着关联（p = 0.029）。本研究结果表明 PIAS3 mRNA 和 miRNA-18a 可能在乳腺癌的发展和发病机制中具有重要意义，这可能反映在针对 STAT3 通路的治疗策略上。然而，需要更大样本量的进一步研究来验证这些观察结果。这可能反映在针对 STAT3 通路的治疗策略上。然而，需要更大样本量的进一步研究来验证这些观察结果。这可能反映在针对 STAT3 通路的治疗策略上。然而，需要更大样本量的进一步研究来验证这些观察结果。