SNHG1/miR‐186/FUT8 regulates cell migration and invasion in oral squamous cell carcinoma

Abstract

Recently, lncRNAs are associated with the progression and development of various cancers. We aimed to explore the effects of lncRNA SNHG1 on the proliferation, apoptosis, migration, and invasion of oral squamous cell carcinoma (OSCC) cells. Quantitative real-time PCR (RT-qPCR) was used for measurement of SNHG1 in OSCC cells. Cell proliferation, apoptosis, migration, and invasion were detected by CCK-8 assay, flow cytometry, Cell Death Detection ELISA PLUS kit, and transwell assays. Dual-luciferase reporter assay and RNA-binding protein immunoprecipitation (RIP) assay were used to clarify the relationship between SNHG1 and miR-186. SNHG1 was overexpressed in OSCC cells. SNHG1 silencing prevented cell proliferation and increased the incidence of apoptosis, DNA fragments, cleaved-caspase 3, and Bax protein levels. Cell migration and invasion were reduced after SNHG1 deletion, and MMP2 and MMP9 protein levels were decreased. SNHG1 overexpression promoted cell survival, migration, and invasion, reduced DNA fragments formation.Mechanistically, we demonstrated that SNHG1 could directly bind to miR-186 and positively regulated α1, 6-fucosyltransferase (FUT8) level. Functional investigation showed that miR-186 depletion reversed the roles of SNHG1 silencing in cell proliferation, apoptosis, and migration. Taken together, our findings illuminated that SNHG1 regulated cell proliferation, migration, and invasion by sponging miR-186 to depress FUT8 expression.

Long non-coding RNA BBOX1-antisense RNA 1 enhances cell proliferation and migration and suppresses apoptosis in oral squamous cell carcinoma via the miR-3940-3p/laminin subunit gamma 2 axis

“…Recently, a transcriptome investigation revealed that long non-coding RNAs (lncRNAs) are putative players in the tumorigenesis of most tumors [ 4 ]. LncRNA SNHG1 expression levels are elevated in OSCC cells and promote tumor cell growth by downregulating the expression of fucosyltransferase 8 by targeting microRNA (miR)-186 [ 5 ]. MYC-induced lncRNA enhances the invasion of OSCC cells by modulating the Wnt/β-catenin pathway [ 6 ].…”

Hsa_circRNA_0001971 contributes to oral squamous cell carcinoma progression via miR‐186‐5p/Fibronectin type III domain containing 3B axis

“…For example, the anticancer roles of miR‐186‐5p were observed in gastric cancer, 25 colorectal cancer, 26 and ovarian cancer. 27 In OSCC, multiple studies found miR‐186 was a tumor suppressor in OSCC by targeting FUT8 28 and SHP2. 29 Here, we for the first time proved that miR‐186‐5p was proved to be downregulated in OSCC samples, and FNDC3B was a target of miR‐186‐5p in OSCC cells.…”

The Multifaceted Role of FUT8 in Tumorigenesis: From Pathways to Potential Clinical Applications

“…In oral squamous cell carcinoma (OSCC), miR-186 has been discovered to directly target and inhibit the expression of FUT8. Nevertheless, a highly expressed lncRNA SNHG1 functions as a sponge for miR-186, counteracting its inhibitory effect and promoting the malignant growth of OSCC [102]. And miR-198 has been found to act directly on the 3 ′ UTR of FUT8 in CRC, thereby reducing FUT8 expression and inhibiting cell proliferation, migration, and invasion [100].…”