Long noncoding RNA HOTAIR promotes breast cancer development through the lncRNA HOTAIR/miR-1/GOLPH3 axis

被引:6
作者
Zhao, Jiawen [1 ]
Zhang, Lei [1 ]
Zhao, Yingzhu [2 ]
Wu, Nan [3 ]
Zhang, Xi [4 ]
Guo, Rong [1 ]
Li, Huimeng [5 ]
Li, Chunxiang [1 ]
Zheng, Kai [1 ]
Liu, Dequan [1 ]
Tang, Shicong [1 ]
机构
[1] Kunming Med Univ, Yunnan Canc Hosp, Affiliated Hosp 3, Dept Breast Surg, Kunming, Peoples R China
[2] Peoples Hosp Guangxi Zhuang Autonomous Reg, Dept Breast & Thyroid Surg, Nanning, Peoples R China
[3] Yunnan Coll Business Management, Dept Med Sch, Kunming, Peoples R China
[4] Yunnan Canc Hosp, Dept Clin Lab, Kunming, Peoples R China
[5] Kunming Med Univ, Southern Cent Hosp Yunnan Prov, Peoples Hosp Honghe State 1, Honghe Hosp,Dept Gen Surg 2, Mengzi, Honghe, Peoples R China
基金
中国国家自然科学基金;
关键词
HOTAIR; miRNA-1; Breast cancer; Proliferation; Migration; MICRORNAS; STABILITY; GOLGI;
D O I
10.1007/s12094-023-03197-3
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
BackgroundThe lncRNA HOTAIR is frequently overexpressed in breast cancer tissues and plays an important role in the development of breast cancer. Here, we investigated the effect of the lncRNA HOTAIR on the biological behaviour of breast cancer cells and its molecular mechanism.MethodsWe investigated the level of HOTAIR in breast cancer and its clinical pathological characteristics by bioinformatic methods. Then, we evaluated the effects of HOTAIR and miRNA-1 expression on the biological behaviour of breast cancer cells by qPCR, Cell Counting Kit-8 (CCK-8) assay, clonogenic assays, Transwell assay and flow cytometry for cell proliferation, invasion migration and apoptosis, and cell cycle analysis. Finally, the target genes of the lncRNA HOTAIR/miR-1/GOLPH3 regulatory axis were validated by luciferase reports.ResultsThe expression of HOTAIR in breast cancer tissues was significantly higher than that in normal breast tissues (P < 0.05). Silencing of HOTAIR suppressed cell proliferation, invasion and migration, promoted apoptosis and induced G(1) phase block in breast cancer (P < 0.0001). We also verified that miR-1 is a target of HOTAIR and that GOLPH3 is a target of miR-1 by luciferase reporter assays (P < 0.001).ConclusionsThe expression of HOTAIR was significantly elevated in breast cancer tissues. Reducing the expression of HOTAIR inhibited the proliferation, invasion and migration of breast cancer cells and promoted apoptosis, and the mechanism was mainly the effect of the lncRNA HOTAIR/miR-1/GOLPH3 regulatory axis on the biological behaviour of breast cancer cells.
引用
收藏
页码:3420 / 3430
页数:11
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