lncRNA SNHG5 promotes cell proliferation, migration and invasion in oral squamous cell carcinoma by sponging miR‑655‑3p/FZD4 axis

Yu, Lijiang; Huo, Lingli; Shao, Xiaolin; Zhao, Juan

doi:10.3892/ol.2020.12173

Cited by 12 publications

(12 citation statements)

References 34 publications

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“…Despite the fact that Transwell and wound healing studies in vitro demonstrated that SNHG5 inhibited migration and invasion of LAD cells, MTS testing revealed no difference in A549 cell proliferation. Therefore, additional research is needed to understand the essential functions of SNHG5 in human cancer [ 33 ]. However, the negative correlation between SNHG5 and several valuable prognostic biomarkers for LAD, including CEA, NSE, and MASP2, and the increased expression of SNHG5 mRNA induced by cisplatin in the previous strongly suggest that SNHG5 might have a therapeutic role in LAD [ 26 ].…”

Section: Discussionmentioning

confidence: 99%

LncRNA SNHG5 Suppresses Cell Migration and Invasion of Human Lung Adenocarcinoma via Regulation of Epithelial-Mesenchymal Transition

Zhang

et al. 2023

Journal of Oncology

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Long noncoding RNAs (lncRNAs) are gradually being annotated as important regulators of multiple cellular processes. The goal of our study was to investigate the effects of the lncRNA small nucleolar RNA host gene 5 (SNHG5) in lung adenocarcinoma (LAD) and its underlying mechanisms. The findings revealed a substantial drop in SNHG5 expression in LAD tissues, which correlated with clinical-pathological parameters. Transcriptome sequencing analysis demonstrated that the inhibitory effect of SNHG5 was associated with cell adhesion molecules. Moreover, the expression of SNHG5 was shown to be correlated with epithelial–mesenchymal transition (EMT) markers in western blots and immunofluorescence. SNHG5 also had significant effects of antimigration and anti-invasion on LAD cells in vitro. Furthermore, the migration and invasion of A549 cells were suppressed by overexpressed SNHG5 in the EMT progress induced by transforming growth factor β1 (TGF-β1), and this might be due to the inhibition of the expression of EMT-associated transcription factors involving Snail, SLUG, and ZEB1. In LAD tissues, the expression of SNHG5 exhibited a positive association with E-cadherin protein expression but a negative correlation with N-cadherin and vimentin, according to the results of quantitative real-time PCR (qRT-PCR). In summary, the current work demonstrated that the lncRNA SNHG5 might limit cell migration and invasion of LAD cancer via decreasing the EMT process, indicating that SNHG5 might be used as a target for LAD therapeutic methods.

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Section: Discussionmentioning

confidence: 99%

LncRNA SNHG5 Suppresses Cell Migration and Invasion of Human Lung Adenocarcinoma via Regulation of Epithelial-Mesenchymal Transition

Zhang

et al. 2023

Journal of Oncology

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“…Recent studies have revealed that lncRNAs are new diagnostic and prognostic biomarkers for various tumors including LUAD [ 9 , 11–15 , 43 , 44 ], and a high expression of the lncRNA EBLN3P is associated with tumor progression [ 16 , 17 , 45 ]. Xu et al indicated that lncRNA EBLN3P promotes colorectal cancer progression by sponging miR-323a-3p [ 16 ].…”

Section: Discussionmentioning

confidence: 99%

The biological function of the long non-coding RNA endogenous born avirus-like nucleoprotein in lung adenocarcinoma is mediated through the microRNA-655-3p/B-cell lymphoma-2 axis

Wang

Yin

2022

Bioengineered

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Lung adenocarcinoma (LUAD) is a subtype of lung cancer, and therapy remains a great challenge. A growing body of evidence shows that long-chain non-coding RNAs (lncRNAs) play an important role in the occurrence and development of LUAD. This study investigated the roles and mechanisms of action of EBLN3P in LUAD. The bioinformatics software starBase and TargetScan were used to predict the binding sites of the lncRNA endogenous born avirus-like nucleoprotein (EBLN3P) and microRNA (miR)-655-3p in LUAD. The regulatory role of EBLN3P and miR-655-3p in cell proliferation was verified through the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2 H-tetrazolium bromide (MTT) assay. The binding sites between EBLN3P, miR-655-3p, and B-cell lymphoma-2 (Bcl-2) were assessed using dual-luciferase reporter assay, western blotting, and quantitative reverse transcription polymerase chain reaction (qRT-PCR). Flow cytometry (FCM) was performed to analyze the apoptotic rates of A549 cells after transfection. The results revealed that EBLN3P was upregulated, whereas miR-655-3p was downregulated in LUAD cell lines (A549 and NCI-H23). Bioinformatics analysis and dual-luciferase reporter assays indicated that EBLN3P interacted with miR-655-3p. Knockdown of EBLN3P notably inhibited the bioactivity and induced apoptosis in A549 cells by upregulating miR-655-3p. Mechanistically, miR-655-3p inhibits cell viability and induces apoptosis by inhibiting Bcl-2 expression. The high expression of Bcl-2 reversed the impact of miR-655-3p on the inhibition of cell bioactivity and induction of apoptosis in A549 cells. In conclusion, this study demonstrated that EBLN3P silencing inhibits bioactivity and induces apoptosis via the miR-655-3p/Bcl-2 axis, providing a potential therapeutic target for lung adenocarcinoma.

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“…Recent study has shown that exosome-carried miR-655-3p is down-regulated in plasma of patients with PTC compared with the healthy group (Liang et al, 2020). MiR-655-3p, an important component for the regulatory network of microRNAs, is identified as a tumor suppressor in multiple cancers, including lung cancer (Wang et al, 2019a), hepatocellular carcinoma (Wu et al, 2016), and oral squamous cell carcinoma (Yu et al, 2020). However, the function and molecular mechanism of exosomal miR-655-3p in PTC have not been reported.…”

Section: Introductionmentioning

confidence: 99%

Exosomal miR-655-3p inhibits growth, and invasion and macrophage M2 polarization through targeting CXCR4 in papillary thyroid carcinoma

et al. 2022

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Papillary thyroid cancer (PTC) is an endocrine malignancy whose incidence has increased rapidly worldwide. Exosome-miR-655-3p was down-regulated in patients with PTC. However, the effect and molecular mechanism of exosome-miR-655-3p in PTC was indistinct until now. Our study found that exosome-miR-655-3p was decreased in serum of PTC patients. Overexpression of miR-655-3p with mimics significantly shrunk the cell viability, reduced the number of chemotactic and invasive PTC cells. Besides, the proportion of CD163 positive cells and the expression of markers of M2 subtype macrophages was markedly decreased when mononuclear macrophage THP-1 was cultured with exosomes of miR-655-3p mimics. Oppositely, the inhibitor of miR-655-3p exacerbated growth, chemotaxis and invasion of PTC cells, and enhanced the M2 subtype macrophages. Structurally, miR-655-3p could target the 3’ untranslated region (3’UTR) of CXCR4 and restrict the expression of CXCR4. In Xenograft tumor experiment, upregulated exosome-miR-655-3p effectively inhibited the growth of tumor and reduced the expression of CXCR4, Ki67 and CD163 in vivo. In summary, exosomal miR-655-3p inhibited growth, invasion and macrophage M2 polarization through targeting CXCR4 in papillary thyroid carcinoma. Regulating exosome-miR-655-3p/CXCR4 may be a potential treatment strategy for PTC.

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lncRNA SNHG5 promotes cell proliferation, migration and invasion in oral squamous cell carcinoma by sponging miR‑655‑3p/FZD4 axis

Cited by 12 publications

References 34 publications

LncRNA SNHG5 Suppresses Cell Migration and Invasion of Human Lung Adenocarcinoma via Regulation of Epithelial-Mesenchymal Transition

LncRNA SNHG5 Suppresses Cell Migration and Invasion of Human Lung Adenocarcinoma via Regulation of Epithelial-Mesenchymal Transition

The biological function of the long non-coding RNA endogenous born avirus-like nucleoprotein in lung adenocarcinoma is mediated through the microRNA-655-3p/B-cell lymphoma-2 axis

Exosomal miR-655-3p inhibits growth, and invasion and macrophage M2 polarization through targeting CXCR4 in papillary thyroid carcinoma

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