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

• Jiawen Zhao ^[1] ; Lei Zhang ^[1] ; Yingzhu Zhao ^[2] ; Nan Wu ^[3] ; Xi Zhang ^[4] ; Rong Guo ^[1] ; Huimeng Li ^[5] ; Chunxiang Li ^[1] ; Kai Zheng ^[1] ; Dequan Liu ^[1] ; Shicong Tang ^[1]
  1. [1] Department of Breast Surgery, The Third Affiliated Hospital of Kunming Medical University, Yunnan Cancer Hospital, Kunming, China
  2. [2] Department of Breast and Thyroid Surgery, The People’s Hospital of Guangxi Zhuang Autonomous Region, Nanning, China
  3. [3] Department of Medical School, Yunnan College of Business Management, Kunming, China
  4. [4] Department of Clinical Laboratory, Yunnan Cancer Hospital, Kunming, China
  5. [5] Second Department of General Surgery, Southern Central Hospital of Yunnan Province, The First People’s Hospital of Honghe State, Honghe Hospital Affiliated to Kunming Medical University, Mengzi, Honghe, China

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• Localización: Clinical & translational oncology, ISSN 1699-048X, Vol. 25, Nº. 12 (December), 2023, págs. 3420-3430
• Idioma: inglés
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• Resumen

  • Background The 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.

    Methods We 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.

    Results The 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 G1 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).

    Conclusions The 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.