Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2018
LINC00511 interacts with miR-765 and modulates tongue squamous cell carcinoma progression by targeting LAMC2.
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Ding Junhai, Yang Changxi, Yang Sen
Аннотация
BACKGROUND: Aimed at underlying the molecular regulatory mechanism and overall biological functions of LINC00511 in tongue squamous cell carcinoma (TSCC).
METHODS: The expression level of LINC00511 was examined by QRT-PCR. In particular, Tca-8113 cell line was selected for subsequent experiments, in which the expression level of LINC00511 was the most significant. Meanwhile, the effects of LINC00511 on cells proliferation, cell cycle distribution, and invasion of TSCC cells were explored using RNA knockdown tools with CCK-8, flow cytometry analysis, colony formation, and transwell assay. Further, bioinformatic analysis and the dual-luciferase reporter assay both were conducted to invalidate the ceRNAs regulatory mechanism of LINC00511 in TSCC.
RESULTS: LINC00511 was obviously upregulated in TSCC tissues and cell lines. Moreover, it was found that LINC00511 served as a competing endogenous RNA (ceRNA) through sponging miR-765 and ultimately modulated the derepression of laminin subunit gamma 2 (LAMC2). The inhibitory effects of miR-765 on TSCC cells proliferation, invasion as well as cell cycle distribution can be restored by the ectopic overexpression of LINC00511. Additionally, the restored capacity of LINC00511 promoted the expression of LAMC2, which was a downstream target of miR-765 and can be negatively regulated by miR-765.
CONCLUSIONS: A novel molecular axis of LINC00511/miR-765/LAMC2 was investigated to regulate the tumor development of TSCC. LINC00511 promoted the expression of LAMC2 via the ceRNA mechanism of sponging miR-765. The ceRNA regulatory network provided a novel understanding of TSCC pathogenesis and also shed light on exploiting the new field of lncRNA-directed therapy against TSCC.
METHODS: The expression level of LINC00511 was examined by QRT-PCR. In particular, Tca-8113 cell line was selected for subsequent experiments, in which the expression level of LINC00511 was the most significant. Meanwhile, the effects of LINC00511 on cells proliferation, cell cycle distribution, and invasion of TSCC cells were explored using RNA knockdown tools with CCK-8, flow cytometry analysis, colony formation, and transwell assay. Further, bioinformatic analysis and the dual-luciferase reporter assay both were conducted to invalidate the ceRNAs regulatory mechanism of LINC00511 in TSCC.
RESULTS: LINC00511 was obviously upregulated in TSCC tissues and cell lines. Moreover, it was found that LINC00511 served as a competing endogenous RNA (ceRNA) through sponging miR-765 and ultimately modulated the derepression of laminin subunit gamma 2 (LAMC2). The inhibitory effects of miR-765 on TSCC cells proliferation, invasion as well as cell cycle distribution can be restored by the ectopic overexpression of LINC00511. Additionally, the restored capacity of LINC00511 promoted the expression of LAMC2, which was a downstream target of miR-765 and can be negatively regulated by miR-765.
CONCLUSIONS: A novel molecular axis of LINC00511/miR-765/LAMC2 was investigated to regulate the tumor development of TSCC. LINC00511 promoted the expression of LAMC2 via the ceRNA mechanism of sponging miR-765. The ceRNA regulatory network provided a novel understanding of TSCC pathogenesis and also shed light on exploiting the new field of lncRNA-directed therapy against TSCC.