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Updated: Feb 22, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
MicroRNA‑509 acts as a tumor suppressor in tongue squamous cell carcinoma by targeting epidermal growth factor
Chao Hou1, Yan Dong2, Fenghe Zhang1
1Shandong Provincial Key Laboratory of Oral Tissue Regeneration, School of Stomatology, Shandong University, Jinan, Shandong 250012, P.R. China.
Abstract:
Tongue squamous cell carcinoma (TSCC) is the most frequent type of oral carcinoma, and is characterized by high metastatic and growth capabilities. Previous studies have demonstrated that aberrantly expressed cancer‑associated microRNAs (miRs) may be associated with tumorigenesis and tumor development in various types of cancer, including TSCC. miR‑509 has been identified as a critical regulator in tumorigenesis and tumor development, via its tumor‑suppressing actions in several types of human cancer. In the present study, miR‑509 expression in TSCC tissues and cell lines was determined by reverse transcription‑quantitative polymerase chain reaction. The effects of miR‑509 on TSCC cell proliferation and invasion were evaluated via MTT and invasion assays, respectively. In addition, the direct target of miR‑509 in TSCC was investigated. The present study demonstrated that miR‑509 expression was downregulated in TSCC tissue samples and cell lines, whereas its ectopic expression suppressed TSCC cell proliferation and invasion in vitro. In addition, epidermal growth factor receptor (EGFR) was identified as a direct target gene of miR‑509 in TSCC cells. EGFR downregulation was demonstrated to suppress the proliferation and invasion of TSCC cells, similar to miR‑509 overexpression. Furthermore, EGFR was significantly upregulated in TSCC tissues, and the levels of miR‑509 were revealed to be negatively correlated with EGFR expression in TSCC tissues. Following transfection with miR‑509 mimics, signaling pathways downstream of EGFR appeared to be suppressed, as phosphorylated (p)‑extracellular signal‑regulated kinase and p‑Akt were downregulated in TSCC cells. In conclusion, the results of the present study suggested that miR‑509 may inhibit the proliferation and invasion of TSCC cells via directly targeting EGFR, thus suggesting that the miR‑509/EGFR axis may have potential as a novel therapeutic target for the development of a treatment for patients with TSCC.
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