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Background: We aimed to demonstrate the regulatory effect of long non‐coding RNA (lncRNA) ENAH‐202 on oral squamous cell carcinoma (OSCC) development as well as its molecular mechanism. Methods: We detected ENAH‐202 expression in OSCC tissues and cell lines by quantitative real‐time PCR (qPCR). The biological function of ENAH‐202 was assessed in vitro and in vivo using CCK‐8, colony formation assays, transwell assays, xenograft formation, and tail vein injection. The further molecular mechanism by which ENAH‐202 promoted OSCC progression was identified using RNA pull‐down, LS‐MS/MS analysis, RNA immunoprecipitation (RIP), and chromatin immunoprecipitation (ChIP) assays. Results: ENAH‐202 was significantly upregulated in OSCC tissues and cells. ENAH‐202 promoted OSCC cell proliferation, migration, and invasion in vitro and in vivo. The expression of enabled homolog (ENAH) and epithelial‐to‐mesenchymal transition (EMT)‐related proteins was changed with the expression of ENAH‐202. Moreover, ENAH‐202 promoted the transcription of Vimentin (VIM) by binding with ZNF502, which can help ENAH‐202 promote OSCC progression. Conclusions: ENAH‐202 facilitated OSCC cell proliferation and metastasis by regulating ZNF502/VIM axis, which played an important role in OSCC progression. [ABSTRACT FROM AUTHOR]

N7‐methylguanosine (m7G) modification is closely related to the occurrence of tumors. However, the m7G modification of circRNAs in oral squamous cell carcinoma (OSCC) remains to be investigated. Methylated RNA immunoprecipitation sequencing (MeRIP‐seq) was used to measure the methylation levels of m7G and identify m7G sites in circRNAs in human OSCC and normal tissues. The host genes of differentially methylated and differentially expressed circRNAs were analyzed by Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, and circRNA–miRNA–mRNA networks were predicted using the miRanda and miRDB databases. The analysis identified 2348 m7G peaks in 624 circRNAs in OSCC tissues. In addition, the source of m7G‐methylated circRNAs in OSCC was mainly the sense overlap region compared with normal tissues. The most conserved m7G motif in OSCC tissues was CCUGU, whereas the most conserved motif in normal tissues was RCCUG (R = G/A). Importantly, GO enrichment and KEGG pathway analysis showed that the host genes of differentially methylated and differentially expressed circRNAs were involved in many cellular biological functions. Furthermore, the significantly differentially expressed circRNAs were analyzed to predict the circRNA–miRNA–mRNA networks. This study revealed the whole profile of circRNAs of differential m7G methylation in OSCC and suggests that m7G‐modified circRNAs may impact the development of OSCC. [ABSTRACT FROM AUTHOR]

Head and neck squamous cell carcinoma (HNSCC) is the most common malignant tumor in the oral and maxillofacial regions, and long noncoding RNAs (lncRNAs) play crucial roles in the occurrence and progression of HNSCC. The lncRNA lnc‐H2AFV‐1 was found to be upregulated in HNSCC tissues; however, the function of lnc‐H2AFV‐1 in regulating HNSCC proliferation and the potential molecular mechanism is unclear. The present study evaluated the expression of lnc‐H2AFV‐1 in HNSCC tissues using quantitative real‐time PCR (qPCR) and associated abundant lnc‐H2AFV‐1 expression with tumor size. Functionally, lnc‐H2AFV‐1 significantly promoted the proliferation of HNSCC cells in vitro and in vivo. Quantified N6‐methyladenosine (m6A) RNA methylation and dot blot assays revealed that total m6A methylation in HNSCC cells was accompanied by lnc‐H2AFV‐1 expression. Western blotting showed that the expression of methyltransferase‐like (METTL) 3 and METTL14 was consistent with that of lnc‐H2AFV‐1, whereas the expression of demethylase fat mass and obesity‐associated (FTO) was contrary to that of lnc‐H2AFV‐1. Methylated RNA immunoprecipitation sequencing (MeRIP‐seq) and MeRIP‐qPCR revealed that lnc‐H2AFV‐1 overexpression led to the elevated expression and maximal m6A methylation of intraflagellar transport (IFT) 80 in HNSCC. In addition, METTL3/14 knockdown decreased IFT80 expression. Thus, our findings suggested that lnc‐H2AFV‐1 might be a biomarker that alters m6A modification by regulating the m6A methylases METTL3/14 and FTO and then mediating the downstream target IFT80 to promote HNSCC progression. [ABSTRACT FROM AUTHOR]

Long non‐coding RNAs (LncRNAs), which are more than 200 nucleotides in length and with limited protein‐coding potential, play vital roles in the pathogenesis, tumorigenesis, and angiogenesis of cancers. Aberrant expression of lncRNAs has been detected in various carcinomas and may be correlated with oncogenesis by affecting related genes expression. Recently, an increasing number of studies have reported on long intergenic non‐protein coding RNA 460 (LINC00460) in human tumor fields. LINC00460 is upregulated in diverse cancer tissues and cells. The upregulated expression level of LINC00460 is correlated with larger tumor size, tumor node metastasis (TNM) stage, lymph node metastasis, and shorter overall survival. The regulatory mechanism of LINC00460 was complex and diverse. LINC00460 could act as a competitive endogenous RNA (ceRNA), directly bind with proteins or regulate multiple pathways, which affected tumor progression. Moreover, LINC00460 was also identified to increase drug resistance, and therefore, weaken the effectiveness of tumor treatment. It has become increasingly important to investigate the roles of LINC00460 in various cancers by different mechanisms. Therefore, a more comprehensive understanding of LINC00460 is crucial to expound on the cellular function and molecular mechanism of human cancers. In this review, we refer to studies concerning LINC00460 and provide the basis for the evaluation of LINC00460 as a predicted biomarker or potential therapeutic target in malignancies, and also provide ideas for the future research of lncRNAs similar to LINC00460. [ABSTRACT FROM AUTHOR]