Open Access

Knockdown of lncRNA‑HOTAIR downregulates the drug‑resistance of breast cancer cells to doxorubicin via the PI3K/AKT/mTOR signaling pathway

  • Authors:
    • Zhixiang Li
    • Jun Qian
    • Jing Li
    • Chao Zhu
  • View Affiliations

  • Published online on: May 29, 2019     https://doi.org/10.3892/etm.2019.7629
  • Pages: 435-442
  • Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

The resistance to chemotherapeutic drugs is a critical feature of breast cancer recurrence and metastasis. Long non‑coding RNAs (LncRNAs) serve key roles in tumor drug resistance. LncRNA‑HOX transcript antisense RNA (HOTAIR) has been reported to be overexpressed in certain types of cancer and may be closely associated with tumor resistance. The current study aimed to investigate the role of lncRNA‑HOTAIR in the regulation of breast cancer resistance to doxorubicin (DOX). A breast cancer cell line (MCF‑7) and DOX‑resistant breast cancer cell line (DOXR‑MCF‑7) were utilized in the current study. DOXR‑MCF‑7 cells were transfected with lncRNA‑HOTAIR small interfering RNA (siRNA) and control siRNA. Subsequently, MTT and colony formation assays were performed to assess cell proliferation. Cell apoptosis was also evaluated via flow cytometry. In addition, western blotting and reverse transcription‑quantitative polymerase chain reaction were performed to detect the expression of caspase‑3, B‑cell lymphoma 2, Bcl‑2‑associated X protein, phosphoinositide 3‑kinase (PI3K), protein kinase B (AKT) and mechanistic target of rapamycin (mTOR), and the phosphorylation of PI3K, AKT, and mTOR. The data indicated that lncRNA‑HOTAIR silencing decreased cell proliferation and increased apoptosis in MCF‑7 and DOXR MCF‑7 cells. Furthermore, lncRNA‑HOTAIR silencing significantly decreased the phosphorylation of PI3K, AKT and mTOR, indicating that the knockdown of lncRNA‑HOTAIR effectively attenuates the resistance of breast cancer cells to DOX by inhibiting the PI3K/AKT/mTOR pathway. In summary, the present study indicated that the knockdown of lncRNA‑HOTAIR weakened the resistance of breast cancer cells to DOX via PI3K/AKT/mTOR signaling, suggesting that lncRNA‑HOTAIR may be a novel intervention target to reverse DOX‑resistance in breast cancer.
View Figures
View References

Related Articles

Journal Cover

July-2019
Volume 18 Issue 1

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Li Z, Qian J, Li J and Zhu C: Knockdown of lncRNA‑HOTAIR downregulates the drug‑resistance of breast cancer cells to doxorubicin via the PI3K/AKT/mTOR signaling pathway. Exp Ther Med 18: 435-442, 2019
APA
Li, Z., Qian, J., Li, J., & Zhu, C. (2019). Knockdown of lncRNA‑HOTAIR downregulates the drug‑resistance of breast cancer cells to doxorubicin via the PI3K/AKT/mTOR signaling pathway. Experimental and Therapeutic Medicine, 18, 435-442. https://doi.org/10.3892/etm.2019.7629
MLA
Li, Z., Qian, J., Li, J., Zhu, C."Knockdown of lncRNA‑HOTAIR downregulates the drug‑resistance of breast cancer cells to doxorubicin via the PI3K/AKT/mTOR signaling pathway". Experimental and Therapeutic Medicine 18.1 (2019): 435-442.
Chicago
Li, Z., Qian, J., Li, J., Zhu, C."Knockdown of lncRNA‑HOTAIR downregulates the drug‑resistance of breast cancer cells to doxorubicin via the PI3K/AKT/mTOR signaling pathway". Experimental and Therapeutic Medicine 18, no. 1 (2019): 435-442. https://doi.org/10.3892/etm.2019.7629