Oral Squamous Cell Cancer

SNHG17[LncRNA]

miR-375[miRNA]

PAX6[mRNA]

OSCC cells

Homo sapiens (human)

Cancer Biomark. 2021;30(1):1-12. doi: 10.3233/CBM-191070.

LncRNA SNHG17 promotes the progression of oral squamous cell carcinoma by modulating miR-375/PAX6 axis.

qRT-PCR;Western blot;Flow Cytometry assay;Luciferase reporter assay;

BACKGROUND: The prognosis of patients with recurrent and/or metastatic oral squamous cell carcinoma (OSCC) remains poor, and its incidence is especially high in developing countries. Multiple long non-coding RNAs (lncRNAs) are recently identified as crucial oncogenic factors or tumor suppressors. This study aimed to probe into the role of lncRNA small nucleolar RNA host gene 17 (SNHG17) on the progression of OSCC. METHODS: The expression level of SNHG17 in OSCC samples was tested using quantitative real-time polymerase chain reaction (qRT-PCR). Human OSCC cell lines CAL-27 and Tca8113 were used in in vitro studies. Cell counting kit-8 (CCK-8) and BrdU assays were used to assess the effect of SNHG17 on OSCC cell proliferation. Flow cytometry was used to study the effect of SNHG17 on OSCC cell apoptosis. Transwell assay was conducted to detect the effect of SNHG17 on migration and invasion. Moreover, luciferase reporter assay was employed to confirm targeting relationship between miR-375 and SNHG17. Additionally, Western blot was used to observe the regulatory function of SNHG17 on PAX6. RESULTS: SNHG17 expression in OSCC clinical samples was significantly increased and was correlated with unfavorable pathological indexes. Its overexpression remarkably accelerated proliferation and metastasis of OSCC cells, while reduced apoptosis. Accordingly, knockdown of SNHG17 suppressed the malignant phenotypes of OSCC cells. Overexpression of SNHG17 significantly reduced the expression of miR-375 by sponging it, but enhanced the expression of PAX6. CONCLUSION: SNHG17 is a sponge of tumor suppressor miR-375 in OSCC, enhances the expression of PAX6 indirectly, and functions as an oncogenic lncRNA.