miR‑375‑3p inhibits the progression of laryngeal squamous cell carcinoma by targeting hepatocyte nuclear factor‑1β
- Kunpeng Chang
- Zhenxing Wei
- Hua Cao
Affiliations: Department of Otolaryngology Head and Neck Surgery, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, Henan 471000, P.R. China, Department of Otolaryngology Head and Neck Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China
- Published online on: August 3, 2020 https://doi.org/10.3892/ol.2020.11941
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et al. This is an open access article distributed under the
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Laryngeal squamous cell carcinoma (LSCC) is one of the most frequently diagnosed head and neck cancers worldwide. Increasing evidence suggests that microRNAs (miRNAs/miRs) regulate the progression of tumorigenesis and the malignant behaviors of cancer cells. The aim of this study was to investigate the function and underlying mechanism of miR‑375‑3p in LSCC. The expression of miR‑375‑3p in LSCC tissues and cells was detected using reverse transcription‑quantitative PCR. The effects of miR‑375‑3p on the malignant phenotype of LSCC cells was determined using the Cell Counting Kit‑8 assay and flow cytometry. The targets of miR‑375‑3p were predicted using the miRDB database and confirmed by the luciferase reporter assay. The results of the present study demonstrated that miR‑375‑3p was downregulated in LSCC tissues and cell lines. Furthermore, overexpression of miR‑375‑3p significantly suppressed the proliferation and cell cycle progression of LSCC cells. Overexpression of miR‑375‑3p also increased LSCC cell apoptosis. Mechanistical analysis indicated that miR‑375‑3p bound the 3'‑untranslated region of the hepatocyte nuclear factor 1β (HNF1β) and decreased its expression in LSCC cells. Consistent with the role of HNF1β in glucose metabolism, overexpression of miR‑375‑3p significantly inhibited glucose consumption and lactate production in LSCC cells. Transfection with HNF1β notably reversed the inhibitory effect of miR‑375‑3p on the proliferation of LSCC cells. Collectively, these results indicate the tumor suppressive role of miR‑375‑3p in LSCC via HNF1β, suggesting that miR‑375‑3p may serve as a potential target in the treatment of LSCC.