Dataset Information

LncRNA LUESCC promotes esophageal squamous cell carcinoma by targeting the miR-6785-5p/NRSN2 axis.

ABSTRACT: Esophageal squamous cell carcinoma (ESCC) is one of the most prevalent gastrointestinal malignancies with high mortality worldwide. Emerging evidence indicates that long noncoding RNAs (lncRNAs) are involved in human cancers, including ESCC. However, the detailed mechanisms of lncRNAs in the regulation of ESCC progression remain incompletely understood. LUESCC was upregulated in ESCC tissues compared with adjacent normal tissues, which was associated with gender, deep invasion, lymph node metastasis, and poor prognosis of ESCC patients. LUESCC was mainly localized in the cytoplasm of ESCC cells. Knockdown of LUESCC inhibited cell proliferation, colony formation, migration, and invasion in vitro and suppressed tumor growth in vivo. Mechanistic investigation indicated that LUESCC functions as a ceRNA by sponging miR-6785-5p to enhance NRSN2 expression, which is critical for the malignant behaviors of ESCC. Furthermore, ASO targeting LUESCC substantially suppressed ESCC both in vitro and in vivo. Collectively, these data demonstrate that LUESCC may exerts its oncogenic role by sponging miR-6785-5p to promote NRSN2 expression in ESCC, providing a potential diagnostic marker and therapeutic target for ESCC patients.

SUBMITTER: Xue ST

PROVIDER: S-EPMC10924007 | biostudies-literature | 2024 Mar

REPOSITORIES: biostudies-literature

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LncRNA LUESCC promotes esophageal squamous cell carcinoma by targeting the miR-6785-5p/NRSN2 axis.

Xue Song-Tao ST Cao Shi-Qiang SQ Ding Jian-Cheng JC Li Wen-Juan WJ Hu Guo-Sheng GS Zheng Jian-Cong JC Lin Xiao X Chen Chun C Liu Wen W Zheng Bin B

Cellular and molecular life sciences : CMLS 20240308 1

Esophageal squamous cell carcinoma (ESCC) is one of the most prevalent gastrointestinal malignancies with high mortality worldwide. Emerging evidence indicates that long noncoding RNAs (lncRNAs) are involved in human cancers, including ESCC. However, the detailed mechanisms of lncRNAs in the regulation of ESCC progression remain incompletely understood. LUESCC was upregulated in ESCC tissues compared with adjacent normal tissues, which was associated with gender, deep invasion, lymph node metast ...[more]

PMID: 38457049

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Project description:Abnormal expression of long-noncoding RNA is involved in the tumorigenesis and progression of various cancers, but the potential molecular regulatory mechanisms are unclear. Microbial flora and chronic inflammation, such as periodontitis, which is associated with oral cancer, affect the occurrence and progression of tumors. Accordingly, we stimulated the tongue squamous cell carcinoma (TSCC) cell lines CAL27 and SCC15 with a low concentration of lipopolysaccharide (LPS) from Porphyromonas gingivalis (P.g) for 6 days and then performed LncRNA sequencing on P.g-LPS-treated CAL27 cells and untreated CAL27 cells. LTSCCAT was upregulated in P.g-LPS-treated CAL27 cells compared with untreated CAL27 cells. LTSCCAT induced epithelial-mesenchymal transition and promoted the invasion and metastasis of TSCC in vitro and in vivo. LncRNA LTSCCAT was upregulated in TSCC patients with periodontitis and was correlated with metastasis and poor prognosis. We predicted through an online database and confirmed by dual-luciferase reporter assays that LTSCCAT is a competitive endogenous RNA for the regulation of miR-103a-2-5p. Another dual-luciferase reporter assay confirmed that miR-103a-2-5p has a binding site at the 3'-UTR of the histone methylation transferase SMYD3 and inhibits its translation. Chromatin immunoprecipitation experiments demonstrated that SMYD3 binds directly to the promoter region of TWIST1 and promotes its transcription, which is related to H3K4 trimethylation. The effect of pcDNA/LTSCCAT on expression was attenuated by miR-103a-2-5p mimics. The RF and SVM classifier predicts that LTSCCAT can bind to SMYD3, whereas the RNA immunoprecipitation (RIP) assay confirms that it cannot. In addition, we predicted the combination of LTSCCAT and SMYD3 through software, but the RIP assay confirmed that LTSCCAT could not be combined with SMYD3. For the first time, we showed that periodontitis promotes the invasion and metastasis of TSCC and clarified the molecular mechanism of LTSCCAT to promote invasion and metastasis of TSCC, providing a potential therapeutic target for clinical treatment of TSCC.

Project description:Esophageal squamous cell carcinoma (ESCC) is one of the most common digestive malignancies. Our previous studies revealed necroptosis-related lncRNA ENSG00000253385.1 was an independent prognostic factor for ESCC. However, the specific regulatory mechanisms are unknown. This study aimed to investigate the expression of the lncRNA ENSG00000253385.1 in ESCC tissues and its relationship with clinicopathological features and patient prognosis, and to explore its potential regulatory mechanism in ESCC cells. We detected the location of the lncRNA ENSG00000253385.1 in ESCC cells by fluorescence in situ hybridization (FISH). FISH and quantitative real-time polymerase chain reaction (qRT‒PCR) were used to detect gene expression in ESCC tissues and cells. Cell proliferation, migration and apoptosis were evaluated by CCK-8 assay, wound healing, transwell cell migration, invasion and flow cytometry assay. The levels of necroptosis-related protein were detected by western blot. The binding sites between miR-16-2-3p and lncRNA ENSG00000253385.1 or voltage-dependent anion channel 1 (VDAC1) were predicted by bioinformatics database and confirmed by dual luciferase reporter gene assay. Results revealed that the lncRNA ENSG00000253385.1 expression was higher in ESCC tissues than in the adjacent tissues. High lncRNA ENSG00000253385.1 expression, positive lymph node metastasis and clinical stage III were associated with poor overall survival (OS) in patients with ESCC, and were independent risk factors for prognosis of patients with ESCC. The lncRNA ENSG00000253385.1 was located in the cytoplasm. MiR-16-2-3p had a direct targeting regulatory relation ship with lncRNA ENSG00000253385.1 and VDAC1. MiR-16-2-3p inhibitor promoted proliferation, migration and invasion, and inhibited apoptosis of ESCC cells. Knockdown of the lncRNA ENSG00000253385.1 could inhibit the proliferation, migration and invasion, promote the apoptosis, and result in increases in the necroptosis-related proteins p-receptor-interacting protein kinase 3 (RIPK3)/RIPK3 and p-mixed lineaae kinase domain-like protein (MLKL)/MLKL and a decrease in the VDAC1 protein levels in ESCC cells, whereas miR-16-2-3p inhibition rescued these effects. Therefore, The lncRNA ENSG00000253385.1/ miR-16-2-3p/VDAC1 axis may be considered as a potential predictive biomarker and target for ESCC.

Dataset Information

LncRNA LUESCC promotes esophageal squamous cell carcinoma by targeting the miR-6785-5p/NRSN2 axis.

Publications

LncRNA LUESCC promotes esophageal squamous cell carcinoma by targeting the miR-6785-5p/NRSN2 axis.

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