Department of Oncology Radiotherapy, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Eur Rev Med Pharmacol Sci. 2021 Oct;25(20):6179-6186. doi: 10.26355/eurrev_202110_26988.
To explore the biological function of long non-coding RNA (lncRNA) MORT in the malignant progression of breast cancer (BCa) and the underlying mechanism, and to provide a novel strategy for clinical treatment.
Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was conducted to detect differential level of MORT in BCa specimens and cell lines. The correlation between MORT level and pathological indexes of BCa patients was analyzed. After intervening MORT level in SKBR-3 and MCF-7 cells, cell viability, migratory rate and wound closure were examined through Cell Counting Kit-8 (CCK-8), transwell and wound healing assay, respectively. Dual-Luciferase reporter assay and rescue experiments were conducted to uncover the regulatory effect of MORT on its target gene FGF1. In vivo function of MORT in mediating tumor growth of BCa was finally assessed by generating a xenograft model in nude mice.
MORT was downregulated in BCa tissues and cell lines. Low level of MORT predicted higher rate of distant metastasis in BCa patients. Overexpression of MORT in SKBR-3 cells reduced proliferative and migratory rates, while knockdown of MORT in MCF-7 enhanced them. Moreover, in vivo overexpression of MORT slowed down tumor growth of BCa in nude mice. MORT could negatively regulate its target gene FGF1, which was responsible for the anti-cancer role of MORT in BCa progression.
MORT is downregulated in BCa specimens, which suppresses proliferative and migratory potentials of BCa cells by negatively regulating FGF1. MORT can be an effective target for precision treatment of BCa.
探索长链非编码 RNA（lncRNA）MORT 在乳腺癌（BCa）恶性进展中的生物学功能及其潜在机制，为临床治疗提供新策略。
采用实时定量聚合酶链反应（qRT-PCR）检测 BCa 标本和细胞系中 MORT 的差异表达水平。分析 MORT 水平与 BCa 患者病理指标的相关性。在 SKBR-3 和 MCF-7 细胞中干预 MORT 水平后，通过细胞计数试剂盒-8（CCK-8）、Transwell 和划痕愈合实验分别检测细胞活力、迁移率和伤口愈合。采用双荧光素酶报告基因和挽救实验揭示 MORT 对其靶基因 FGF1 的调控作用。最后，通过在裸鼠中建立异种移植模型评估 MORT 在介导 BCa 肿瘤生长中的体内功能。
MORT 在 BCa 组织和细胞系中表达下调。MORT 低表达预示着 BCa 患者远处转移的发生率更高。在 SKBR-3 细胞中过表达 MORT 降低了增殖和迁移率，而在 MCF-7 细胞中敲低 MORT 则增强了这些作用。此外，在裸鼠中过表达 MORT 可减缓 BCa 肿瘤的生长。MORT 可负向调控其靶基因 FGF1，这是 MORT 在 BCa 进展中发挥抗癌作用的原因。
MORT 在 BCa 标本中表达下调，通过负向调控 FGF1 抑制 BCa 细胞的增殖和迁移潜能。MORT 可作为 BCa 精准治疗的有效靶点。
