Long non‑coding RNA MIR4435‑2HG promotes the progression of head and neck squamous cell carcinoma by regulating the miR‑383‑5p/RBM3 axis
- Shu Wang
- Xianfeng Chen
- Tiankui Qiao
Affiliations: Center for Tumor Diagnosis and Therapy, Jinshan Hospital, Fudan University, Shanghai 201508, P.R. China, Department of Pharmacy, Tinglin Hospital, Shanghai 201505, P.R. China
- Published online on: April 13, 2021 https://doi.org/10.3892/or.2021.8050
Copyright: © Wang
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Recent studies have shown that long non‑coding RNAs (lncRNAs) are strongly related to the progression of various types of cancer. The lncRNA MIR4435‑2 host gene (MIR4435‑2HG) has been recently recognized as a tumor‑related lncRNA that is upregulated in several tumors. However, its possible functions in head and neck squamous cell carcinoma (HNSCC) remain unclear. In tShe present study, we observed that MIR4435‑2HG expression was markedly upregulated in HNSCC tissues based on a Gene Expression Profiling Interactive Analysis dataset. This result was further confirmed in HNSCC tissues and cell lines using quantitative real‑time polymerase chain reaction. In addition, the high expression level of MIR4435‑2HG was significantly associated with poor disease‑free survival and overall survival in all HNSCC cases and was associated with advanced tumor‑metastasis‑node stage and poor prognosis. In vitro and in vivo assays demonstrated that MIR4435‑2HG knockdown suppressed HNSCC cell proliferation and invasion, epithelial‑mesenchymal transition (EMT), and tumor growth as determined by Cell Counting Kit‑8, Transwell assays and western blotting. Furthermore, MIR4435‑2HG affected HNSCC cell proliferation and migration and EMT by modulating the microRNA miR‑383‑5p to positively regulate the protein expression level of RNA‑binding motif protein 3 (RBM3). In conclusion, we provide a detailed analysis of the roles of MIR4435‑2HG in HNSCC and identified the MIR4435‑2HG/miR‑383‑5p/RBM3 axis as a potential therapeutic target for HNSCC treatment.