Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2021
Wnt/β-catenin signaling pathway participates in the effect of miR-626 on oral squamous cell carcinoma by targeting RASSF4.
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Cui Sheng-Hai, Hu Xiao-Di, Yan Yan
Аннотация
BACKGROUND: The role of miR-626 in oral squamous cell carcinoma (OSCC) was investigated by targeting RASSF4.
METHODS: The miR-626 and RASSF4 expression was detected in normal oral mucosa or OSCC tissues and OSCC or normal cells. The methylation status of RASSF4 was analyzed using methylation-specific polymerase chain reaction (PCR). The cytoplasmic/nuclear ratios (C/N ratios) targeted by miR-626 were examined using microarray, followed by a dual-luciferase reporter assay. The subcellular localization of RASSF4 and miR-626 in OSCC cells was determined using RNA fluorescence in situ hybridization (FISH) and immunocytochemistry (ICC), respectively. Ca9-22 and HSC2 cells were divided into mock, inhibitor NC, miR-626 inhibitor, scramble, RASSF4 and miR-626 mimic + RASSF4 groups, and then CCK-8, Annexin V-FITC/PI, wound healing, Transwell, qRT-PCR and western blotting assays were performed.
RESULTS: OSCC tissues and cells had increased miR-626 expression and decreased RASSF4 expression. Patients with RASSF4 methylation had lower RASSF4 expression than those without methylation. In addition, a negative correlation between miR-626 and RASSF4 was found in OSCC tissues, both of which were correlated with the pathological grade, pathological stage, lymph node metastasis and patient prognosis. MiR-626 targeted RASSF4 in OSCC cells. Overexpressed RASSF4 inhibited the proliferation, invasion, migration and epithelial-mesenchymal transition (EMT) of OSCC cells, promoted cell apoptosis, and blocked the Wnt/β-Catenin pathway, which was reversed by miR-626 overexpression.
CONCLUSIONS: Inhibiting miR-626 can regulate the biological characteristics of OSCC cells, including proliferation, invasion, migration, EMT and apoptosis, by targeting RASSF4, which may be related to the Wnt/β-Catenin pathway.
METHODS: The miR-626 and RASSF4 expression was detected in normal oral mucosa or OSCC tissues and OSCC or normal cells. The methylation status of RASSF4 was analyzed using methylation-specific polymerase chain reaction (PCR). The cytoplasmic/nuclear ratios (C/N ratios) targeted by miR-626 were examined using microarray, followed by a dual-luciferase reporter assay. The subcellular localization of RASSF4 and miR-626 in OSCC cells was determined using RNA fluorescence in situ hybridization (FISH) and immunocytochemistry (ICC), respectively. Ca9-22 and HSC2 cells were divided into mock, inhibitor NC, miR-626 inhibitor, scramble, RASSF4 and miR-626 mimic + RASSF4 groups, and then CCK-8, Annexin V-FITC/PI, wound healing, Transwell, qRT-PCR and western blotting assays were performed.
RESULTS: OSCC tissues and cells had increased miR-626 expression and decreased RASSF4 expression. Patients with RASSF4 methylation had lower RASSF4 expression than those without methylation. In addition, a negative correlation between miR-626 and RASSF4 was found in OSCC tissues, both of which were correlated with the pathological grade, pathological stage, lymph node metastasis and patient prognosis. MiR-626 targeted RASSF4 in OSCC cells. Overexpressed RASSF4 inhibited the proliferation, invasion, migration and epithelial-mesenchymal transition (EMT) of OSCC cells, promoted cell apoptosis, and blocked the Wnt/β-Catenin pathway, which was reversed by miR-626 overexpression.
CONCLUSIONS: Inhibiting miR-626 can regulate the biological characteristics of OSCC cells, including proliferation, invasion, migration, EMT and apoptosis, by targeting RASSF4, which may be related to the Wnt/β-Catenin pathway.