Long noncoding RNA HOTAIR promotes the proliferation and metastasis of osteosarcoma cells through the AKT/mTOR signaling pathway
- Enqi Li
- Zhe Zhao
- Baotong Ma
- Jinli Zhang
Published online on: October 2, 2017
Copyright: © Li et al.
This is an open access article distributed under the terms of Creative Commons Attribution License.
It has been proven that long non‑coding (lnc)RNAs serve an important role in the tumorigenesis and development of several types of human malignancy. Previous studies have demonstrated that the lncRNA Hox transcript antisense intergenic RNA (HOTAIR) is involved in the development various types of cancer, including osteosarcoma (OS). However, the underlying mechanisms by which it has an affect are still largely unknown. In the present study, it was observed that the expression of HOTAIR was significantly upregulated in OS tissues compared to matched adjacent normal tissues, using reverse transcription‑quantitative polymerase chain reaction analysis. HOTAIR was silenced using specific small interfering RNA (siRNA/siR), siR‑HOTAIR, in order to investigate its role in regulating OS cell proliferation, apoptosis, migration and invasion. siR‑HOTAIR inhibited the proliferation of MG‑63 cells due to the induction of G1 phase arrest. In addition, the results of in vitro assays demonstrated that the suppression of HOTAIR in MG‑63 OS cells significantly reduced migration and invasion. The silencing of HOTAIR also significantly decreased the expression of matrix metalloproteinase (MMP) 2 and MMP9, but increased E‑cadherin expression through regulating the RAC α serine/threonine protein kinase‑mammalian target of rapamycin signaling pathway. The results indicated that siR‑HOTAIR may be a potential OS therapy.