微小RNA-675通过抑制上皮-间质转化和转化生长因子β信号传导来抑制原发性卵巢肿瘤的生长和转移。

MiR-675 Inhibits Primary Ovarian Tumor Growth and Metastasis by Suppressing EMT and TGFβ Signaling.

作者信息

Zhao Xinxin, Liu Ziping, Li Yongshuai, Song Shiji, Wang Baojin, Pfeffer Lawrence M, Zhang Wenjing, Yue Junming

机构信息

Department of Gynecology and Obstetrics, the Third Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 450052, China.

Department of Pathology and Laboratory Medicine, College of Medicine, the University of Tennessee Health Science Center, Memphis, TN, 38163, USA.

出版信息

J Cancer. 2025 Jan 1;16(1):55-65. doi: 10.7150/jca.102654. eCollection 2025.

DOI:10.7150/jca.102654

PMID:39744561

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11660139/

Abstract

MicroRNAs (miRNAs) can function as either tumor suppressors or oncogenes. This study explores the role of miR-675 in ovarian cancer (OC) using OC cell lines and an orthotopic mouse model. We demonstrate that miR-675 expression inhibits primary tumor growth and metastasis by targeting TGFβ1, suppressing epithelial to mesenchymal transition (EMT), and attenuating the TGFβ signaling pathway. Functional assays revealed significant inhibition of cell proliferation, migration, and invasion by miR-675. In addition, miR-675 synergistically enhanced the apoptotic effect of paclitaxel and carboplatin, suggesting potential for combination therapy of miRNA-675 with chemotherapeutic agents. studies using orthotopic injection of miR-675 expressing and control OC cells in NSG mice demonstrated significant inhibition of primary OC growth and metastasis. These findings indicate that miR-675 is a promising therapeutic target for OC treatment.

摘要

微小RNA（miRNA）可作为肿瘤抑制因子或癌基因发挥作用。本研究利用卵巢癌细胞系和原位小鼠模型，探讨了miR-675在卵巢癌（OC）中的作用。我们证明，miR-675通过靶向转化生长因子β1（TGFβ1）、抑制上皮-间质转化（EMT）以及减弱TGFβ信号通路来抑制原发性肿瘤生长和转移。功能试验显示，miR-675对细胞增殖、迁移和侵袭有显著抑制作用。此外，miR-675协同增强了紫杉醇和卡铂的凋亡效应，提示miR-675与化疗药物联合治疗具有潜力。在NSG小鼠中进行的原位注射表达miR-675的OC细胞和对照OC细胞的研究表明，原发性OC的生长和转移受到显著抑制。这些发现表明，miR-675是OC治疗中一个有前景的治疗靶点。