MALAT1 knockdown inhibits hypopharyngeal squamous cell carcinoma malignancy by targeting microRNA‑194
- Hongming Wang
- Fei Wang
- Wenyu Ouyang
- Xuejun Jiang
- Wei Li
Affiliations: Department of Otolaryngology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China
- Published online on: April 21, 2020 https://doi.org/10.3892/ol.2020.11551
Copyright: © Wang
et al. This is an open access article distributed under the
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Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in the oncogenesis and progression of various types of cancer. However, the function of MALAT1 in hypopharyngeal squamous cell carcinoma (HSCC) is not completely understood. In the present study, MALAT1 expression levels were determined using reverse transcription‑quantitative PCR, and Cell Counting Kit‑8, Transwell and flow cytometry assays were performed to investigate the biological functions of HSCC cells. The results indicated that MALAT1 was upregulated in HSCC. MALAT1 knockdown suppressed HSCC cell proliferation, migration and invasion, and promoted apoptosis compared with the control group. Additionally, microRNA (miR)‑194 was identified as a target of MALAT1 and was expressed at low levels in HSCC tissues compared with adjacent non‑tumor tissues. A miR‑194 agomir inhibited malignant cell behaviors, including cell proliferation, migration and invasion, whereas miR‑194 antagomir promoted malignant behaviors compared with the corresponding control groups. In addition, the results suggested that MALAT1 knockdown inhibited the malignant behaviors of HSCC cells by binding miR‑194. miR‑194 inhibition partially reversed the MALAT1 knockdown‑induced inhibitory effects on HSCC cells. Furthermore, MALAT1 knockdown combined with miR194 mimics resulted in the lowest tumor volume among all tested groups in vivo. In conclusion, the results of the present study suggested that MALAT1 knockdown suppressed the malignant behavior of HSCC by targeting miR‑194; therefore, MALAT1 may serve as a novel therapeutic target for HSCC.