Background: Maternally expressed 3 (MEG3), a long chain noncoding RNA (lncRNA), has verified its function as a suppressor in several kinds of cancers. However, the downstream mechanism of MEG3 in regulating the molecular mechanism of epithelial-mesenchymal transformation (EMT) in head and neck squamous cell carcinoma (HNSCC) progression demands further investigation. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expression level of MEG3 in HNSCC and adjacent normal tissues of 51 cases. Luciferase report assay was used to detect the correlation between miR-421 and MEG3, and miR-421 and E-cadherin in HNSCC cell lines. Cell invasion and proliferation capacity were assessed through transwell and CCK8 assays. Scratch wound assay was used to assess cell migration capacity. Results: Firstly, this study demonstrated that the expression of MEG3 was significantly downregulated in HNSCC compared to adjacent normal tissues. Overexpressed MEG3 inhibited cell proliferation, migration, and invasion in vitro. Secondly, MEG3 upregulated the expression of E-cadherin, which was instead downregulated by miR-421. MiR-421 was negatively regulated by MEG3 in HNSCC. Therefore, MEG3 regulated EMT by sponging miR-421 targeting E-cadherin in HNSCC. Conclusions: This study indicated that the MEG3-miR-421-E-cadherin axis could be a new therapeutic target for HNSCC. K E Y W O R D S epithelial-mesenchymal transition, head and neck squamous cell carcinoma, maternally expressed 3, miR-421

Objective Long non‐coding RNA (lncRNA) MEG3 was associated with multiple types of cancers such as oral squamous cell carcinoma (OSCC). Single nucleotide polymorphisms (SNPs) might affect cancer risk by modifying the function of lncRNAs. But fewer study researched the relationship between SNPs and MEG3 in cancers. Considering these reasons, we supposed SNPs in MEG3 may influence the risk of OSCC. Material and Methods The selected SNPs in MEG3 were genotyped in 1,428 subjects (444 patients with OSCC and 984 cancer‐free controls). The relationship between SNPs in MEG3 and OSCC risk was calculated by logistic regression analysis. The function of the SNPs was explored by luciferase activity assay. Results A statistically significant increased risk was observed between rs11160608 and OSCC (Dominant model: adjusted OR = 1.36, 95% CI = 1.06–1.76, p = 0.017). Moreover, the effect of rs11160608 CC genotype with OSCC risk was much strong in drinkers than non‐drinkers (adjusted OR = 1.79, 95% CI = 1.17–2.73, p = 0.007). Furthermore, the luciferase activity of rs11160608 A allele was lower than rs11160608 C allele by luciferase reporter assay. Conclusion Our study confirmed that the SNP rs11160608 in MEG3 might play an important role in OSCC by interring the binding of miRNA.

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This study aimed to explore the function of CLPTM1L in oral squamous cell carcinoma and mechanism of tumorigenesis. The expression of CLPTM1L was detected by immunohistochemistry. The localization in cells was detected by immunofluorescence. Cell invasion, proliferation, and migration were detected by transwell, CCK-8 and scratch-wound test. The possible characteristics of CLPTM1L were analysed in TCGA, GO, KEGG and String databases. IHC revealed that the expression of CLPTM1L in 92 cases of OSCC tissues was significantly higher ( P < 0.01) than 29 cases of normal oral epithelium tissues. The expression of CLPTM1L was significantly higher in oral squamous cell carcinoma in TCGA database. CLPTM1L expression was not significantly correlated with the patients’ clinical parameters. High expression of CLPTM1L was associated with worse prognosis. Cox regression analysis demonstrated that the CLPTM1L expression was the significant risk factor. CLPTM1L was mainly localized in the perinuclear cytoplasm. The vitro studies revealed that the knockdown of CLPTM1L suppressed invasion, proliferation and migration. CLPTM1L related genes were enriched in protein processing in the endoplasmic reticulum, protein folding, endoplasmic reticulum formation, N-glycan biosynthesis, and protein hydroxylation. Highly expressed CLPTM1L may contribute to a poor prognosis and increase invasion, proliferation and migration of oral squamous cell carcinoma. CLPTM1L may play an important role in tumorgenesis and would be a valuable target gene for the treatment of oral squamous cell carcinoma.

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