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DLEU1 promotes oral squamous cell carcinoma progression by activating interferon-stimulated genes
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DLEU1 promotes oral squamous cell carcinoma progression by activating interferon-stimulated genes
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Journal Article
DLEU1 promotes oral squamous cell carcinoma progression by activating interferon-stimulated genes
2021
Overview
Long noncoding RNAs (lncRNAs) are deeply involved in cancer development. We previously reported that DLEU1 (deleted in lymphocytic leukemia 1) is one of the lncRNAs overexpressed in oral squamous cell carcinoma (OSCC) cells, where it exhibits oncogenic activity. In the present study, we further clarified the molecular function of DLEU1 in the pathogenesis of OSCC. Chromatin immunoprecipitation-sequencing (ChIP-seq) analysis revealed that DLEU1 knockdown induced significant changes in the levels of histone H3 lysine 4 trimethylation (H3K4me3) and H3K27 acetylation (H3K27ac) in OSCC cells. Notably, DLEU1 knockdown suppressed levels of H3K4me3/ H3K27ac and expression of a number of interferon-stimulated genes (ISGs), including IFIT1, IFI6 and OAS1, while ectopic DLEU1 expression activated these genes. Western blot analysis and reporter assays suggested that DLEU1 upregulates ISGs through activation of JAK-STAT signaling in OSCC cells. Moreover, IFITM1, one of the ISGs induced by DLUE1, was frequently overexpressed in primary OSCC tumors, and its knockdown inhibited OSCC cell proliferation, migration and invasion. These findings suggest that DLEU1 exerts its oncogenic effects, at least in part, through activation of a series ISGs in OSCC cells.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ Antigens, Differentiation - metabolism
/ Carcinoma, Squamous Cell - metabolism
/ Carcinoma, Squamous Cell - pathology
/ Gene Expression Regulation, Neoplastic
/ Genomes
/ Histones
/ Humanities and Social Sciences
/ Humans
/ Kinases
/ Leukemia
/ Lysine
/ Medicine
/ Mouth Neoplasms - metabolism
/ Oral squamous cell carcinoma
/ Receptors, Interferon - metabolism
/ RNA, Long Noncoding - metabolism
/ RNA, Long Noncoding - physiology
/ Science
/ STAT1 Transcription Factor - metabolism
/ Tumors
