scholarly journals LncRNA NEAT1 Regulates Cell Viability and Invasion in Esophageal Squamous Cell Carcinoma through the miR-129/CTBP2 Axis

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Yong Li ◽  
Dong Chen ◽  
Xiang Gao ◽  
Xiaohui Li ◽  
Gongning Shi
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Viability ◽  
Cell Carcinoma ◽  
Molecular Mechanism ◽  
Squamous Cell ◽  
Noncoding Rna ◽  
Luciferase Reporter ◽  
Cell Progression ◽  
Lncrna Neat1

Background. Long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) was reported to be aberrantly upregulated and promote esophageal squamous cell carcinoma (ESCC) cell progression. Nevertheless, the molecular mechanism of NEAT1 involved in the competing endogenous RNA (ceRNA) regulatory network in ESCC progression remains poorly defined. Methods. The expressions of NEAT1, miR-129, and C-terminal-binding protein 2 (CTBP2) in ESCC cells were examined by qRT-PCR. The effects of NEAT1 knockdown and miR-129 overexpression, or along with CTBP2 upregulation, on ESCC cell viability and invasion were explored by CCK-8 and transwell invasion assays, respectively. Luciferase reporter assay in combination with RIP was performed to confirm the interaction between NEAT1, miR-129, and CTBP2. Results. NEAT1 and CTBP2 were upregulated and miR-129 was downregulated in ESCC cells. Either NEAT1 knockdown or miR-129 overexpression suppressed ESCC cell viability and invasion. Moreover, NEAT1 functioned as an endogenous sponge to downregulate miR-129 by competitively binding to miR-129, thereby leading to the derepression of CTBP2, a target of miR-129. CTBP2 restoration overturned cell viability and invasion suppression mediated by NEAT1 knockdown or miR-129 overexpression. Conclusion. LncRNA NEAT1 regulated ESCC cell viability and invasion via the miR-129/CTBP2 axis, contributing to the better understanding of the molecular mechanism of ESCC pathogenesis and progression.

scholarly journals LncRNA GACAT3 promotes esophageal squamous cell carcinoma progression through regulation of miR-149/FOXM1

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Min Su ◽  
Jinming Tang ◽  
Baihua Zhang ◽  
Desong Yang ◽  
Zhining Wu ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Colony Formation ◽  
Noncoding Rna ◽  
Xenograft Model ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Foxm1 Expression

Abstract Background The long noncoding RNA gastric cancer associated transcript 3 (GACAT3) has been demonstrated to be implicated in the carcinogenesis and progression of many malignancies. However, GACAT3’s levels and role in esophageal squamous cell carcinoma (ESCC) has not been elucidated. Methods GACAT3 amounts were investigated in ESCC tissues and cell lines by qPCR. Its biological functions were examined by CCK-8 assay, colony formation assay, flow cytometry, wound healing assay, transwell assay, and xenograft model establishment. The relationship between GACAT3 and miR-149 was assessed by dual-luciferase reporter assay. Results GACAT3 amounts were elevated in ESCC tissue and cell specimens. Functional studies showed that GACAT3 silencing reduced the proliferation, migration and invasion of cultured ESCC cells, and decreased tumor growth in mice. Furthermore, GACAT could directly interact with miR-149. In addition, colony formation and invasion assays verified that GACAT3 promotes ESCC tumor progression through miR-149. Moreover, GACAT3 acted as a competing endogenous RNA (ceRNA) to modulate FOXM1 expression. Conclusions These findings indicate that GACAT3 functions as an oncogene by acting as a ceRNA for miR-149 to modulate FOXM1 expression in ESCC, suggesting that GACAT3 might constitute a therapeutic target in ESCC.

scholarly journals LncRNA GACAT3 promotes esophageal squamous cell carcinoma progression through regulation of miR-149 /FOXM1

2021 ◽  
Author(s):  
Min Su ◽  
Jinming Tang ◽  
Baihua Zhang ◽  
Desong Yang ◽  
Zhining Wu ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Colony Formation ◽  
Noncoding Rna ◽  
Xenograft Model ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Foxm1 Expression

Abstract Background The long noncoding RNA gastric cancer associated transcript 3 (GACAT3) has been demonstrated to be implicated in the carcinogenesis and progression of many malignancies. However, GACAT3’s levels and role in esophageal squamous cell carcinoma (ESCC) has not been elucidated. Methods GACAT3 amounts were investigated in ESCC tissues and cell lines by qPCR. Its biological functions were examined by CCK-8 assay, colony formation assay, flow cytometry, wound healing assay, transwell assay, and xenograft model establishment. The relationship between GACAT3 and miR-149 was assessed by dual-luciferase reporter assay. Results GACAT3 amounts were elevated in ESCC tissue and cell specimens. Functional studies showed that GACAT3 silencing reduced the proliferation, migration and invasion of cultured ESCC cells, and decreased tumor growth in mice. Furthermore, GACAT could directly interact with miR-149. In addition, colony formation and invasion assays verified that GACAT3 promotes ESCC tumor progression through miR-149. Moreover, GACAT3 acted as a competing endogenous RNA (ceRNA) to modulate FOXM1 expression. Conclusions These findings indicate that GACAT3 functions as an oncogene by acting as a ceRNA for miR-149 to modulate FOXM1 expression in ESCC, suggesting that GACAT3 might constitute a therapeutic target in ESCC.

scholarly journals Long Noncoding RNA Nuclear Paraspeckle Assembly Transcript 1 Promotes Progression and Angiogenesis of Esophageal Squamous Cell Carcinoma Through miR-590-3p/MDM2 Axis

2021 ◽  
Vol 10 ◽  
Author(s):  
Jing Luo ◽  
Kai Xie ◽  
Xiang Gao ◽  
Yu Yao ◽  
Gaoming Wang ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Noncoding Rna ◽  
High Throughput Sequencing ◽  
Mdm2 Expression ◽  
Xenograft Models ◽  
Lncrna Neat1

Angiogenesis has been identified as one of the hallmarks of cancer and aggravates cancer development and progression. Accumulating evidence indicated that long noncoding RNAs (lncRNAs) are powerful factors in regulating various cancer behaviors. The aim of this study is to verify the function and potential mechanisms of lncRNA NEAT1 in progression and angiogenesis of esophageal squamous cell carcinoma (ESCC). We found that NEAT1 was overexpressed in ESCC tissues and correlated with clinical characteristics of patients. Silence of NEAT1 inhibited proliferation, migration, invasion and angiogenesis of ESCC cells. High throughput sequencing and western blotting revealed that NEAT1 regulated MDM2/p53 pathway. Rescue of MDM2 restored the effect of NEAT1 on progression and angiogenesis of ESCC cells. Nude mice xenograft models further validated the role of NEAT1 in vivo. Importantly, NEAT1 functioned as a competing endogenous RNA for miR-590-3p to regulate MDM2 expression and miR-590-3p acted as a tumor suppressor in ESCC progression and angiogenesis. These findings suggested that NEAT1/miR-590-3p/MDM2 axis might serve as potential therapeutic targets for ESCC patients.

Ginsenoside 20(S)-Rg3 suppresses cell viability in esophageal squamous cell carcinoma via modulating miR-324-5p-targeted PSME3

2021 ◽  
pp. 096032712110173
Author(s):  
Min Jiang ◽  
Yinxing Zhu ◽  
Hong Yu
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Viability ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Target Gene ◽  
Luciferase Reporter ◽  
Flow Cytometry Analysis ◽  
Proteasome Activator ◽  
Reporter Assays

Ginsenoside 20(S)-Rg3 is identified as an active saponin monomer which derived from red ginseng and is demonstrated to play an anti-tumor role in diverse cancers. MicroRNAs (miRNAs) are important regulators in the progression of cancers, containing esophageal squamous cell carcinoma (ESCC). It was reported that microRNA 324-5p (miR-324-5p) exerted critical functions in some cancers; however, the detailed molecular mechanism of miR-324-5p mediated by 20(S)-Rg3 to suppress cell viability in ESCC has not been explored. Herein, we explored the function of 20(S)-Rg3 or miR-324-5p on ESCC cell viability by MTT assay, colony formation assay, flow cytometry analysis and western blot analysis. The binding of miR-324-5p to its target gene, proteasome activator subunit 3 (PSME3), was confirmed through RNA pull down and luciferase reporter assays. The results indicated that 20(S)-Rg3 significantly inhibited cell viability and the cell cycle and facilitated cell apoptosis. Furthermore, this effect was strengthened with the increased concentration of 20(S)-Rg3. Moreover, we found that miR-324-5p level was increased under 20(S)-Rg3 treatment. Additionally, overexpressed miR-324-5p inhibited ESCC cell viability, and downregulated miR-324-5p recovered inhibited cell viability caused by 20(S)-Rg3. Further exploration verified that miR-324-5p targeted PSME3, and PSME3 deficiency countervailed the effect of miR-324-5p inhibition on ESCC cell viability under 20(S)-Rg3 treatment. Conclusively, 20(S)-Rg3 suppresses cell viability in ESCC via mediating miR-324-5p-targeted PSME3.

scholarly journals Lnc-PICSAR contributes to cisplatin resistance by miR-485-5p/REV3L axis in cutaneous squamous cell carcinoma

2020 ◽  
Vol 15 (1) ◽  
pp. 488-500
Author(s):  
Dan Wang ◽  
Xiaoqiang Zhou ◽  
Jing Yin ◽  
Yang Zhou
Keyword(s):  
Drug Resistance ◽  
Squamous Cell Carcinoma ◽  
Cell Viability ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Cutaneous Squamous Cell Carcinoma ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cell Progression

AbstractBackgroundDysregulation of long noncoding RNAs (lncRNAs) is associated with drug resistance in multiple cancers. We explored the roles of lncRNA p38 inhibited cutaneous squamous cell carcinoma-associated lincRNA (PICSAR) in cisplatin (DDP) resistance of cutaneous squamous cell carcinoma (CSCC).MethodsQuantitative real-time polymerase chain reaction (qRT-PCR) was employed to measure the expression of lnc-PICSAR, miR-485-5p and reversionless 3-like (REV3L) mRNA. The cell counting kit-8 (CCK-8) assay was conducted to evaluate DDP resistance and cell viability. The transwell assay was performed to determine cell migration and invasion. Western blot assay and immunohistochemistry (IHC) staining assay were carried out to measure protein levels. The dual-luciferase reporter assay was used to investigate the association between miR-485-5p and lnc-PICSAR or REV3L. Murine xenograft model was constructed to explore the function of lnc-PICSAR in vivo. The morphology of exosomes was analyzed by transmission electron microscopy (TEM) and nanoparticle tracking analysis (NTA).ResultsLnc-PICSAR was elevated in DDP-resistant CSCC cells. Lnc-PICSAR silencing suppressed cell viability, DDP resistance, migration and invasion in DDP-resistant CSCC cells. MiR-485-5p acted as a target of lnc-PICSAR, and miR-485-5p inhibition reversed the impacts of lnc-PICSAR silencing on DDP resistance and cell progression in DDP-resistant CSCC cells. Lnc-PICSAR promoted REV3L expression via sponging miR-485-5p. Moreover, REV3L overexpression overturned the effects of lnc-PICSAR on cell progression and DDP resistance. Lnc-PICSAR knockdown suppressed DDP resistance in vivo. In addition, lnc-PICSAR was increased in the exosomes derived from CSCC patients’ serum and CSCC cells.ConclusionLnc-PICSAR enhanced DDP resistance via miR-485-5p/REV3L axis in DDP-resistant CSCC cells. Besides, exosome-mediated lnc-PICSAR might be involved in the regulation of drug resistance in CSCC.

scholarly journals High expression of the long noncoding RNA SH3PXD2A-AS1 is associated with poor prognosis in patients with esophageal squamous cell carcinoma

2020 ◽  
Vol 48 (9) ◽  
pp. 030006052094905
Author(s):  
Qiuli Luo ◽  
Shanshan Wang ◽  
Haibo Han ◽  
Fei Xie ◽  
Jinfeng Chen
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Viability ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
High Expression ◽  
Migration And Invasion ◽  
Poor Prognostic Factor

Objective Our objective was to explore the prognostic role of long noncoding RNA (lncRNA) SH3PXD2A-AS1 in esophageal squamous cell carcinoma (ESCC). Methods An SH3PXD2A-AS1 expression dataset was retrieved and analyzed from The Cancer Genome Atlas database, and SH3PXD2A-AS1 expression was determined in our cohort of 134 ESCC patients by using quantitative PCR. The clinical significance of SH3PXD2A-AS1 expression was investigated by the Chi square test and its prognostic value was determined by Kaplan–Meier survival curve analysis and Cox proportional hazards analysis. RNA interference and in vitro functional experiments, including cell viability, migration, and invasion, were used to investigate effects of SH3PXD2A-AS1 on cell malignant phenotype. Results SH3PXD2A-AS1 expression was increased in ESCC tissues compared with adjacent normal tissues. A high level of SH3PXD2A-AS1 expression was associated with poor tumor differentiation and advanced T, N, and TNM stages, indicating its oncogenic role in ESCC. Moreover, its high expression predicted poor overall survival in patients with ESCC. Inhibition of SH3PXD2A-AS1 expression significantly suppressed cell viability, migration, and invasion of ESCC cells. Conclusion High SH3PXD2A-AS1 expression is a poor prognostic factor for patients with ESCC. SH3PXD2A-AS1 might function as an oncogene that can promote malignant biological characteristics of ESCC cells.

scholarly journals LncRNA FOXP4-AS1 Promotes the Progression of Esophageal Squamous Cell Carcinoma by Interacting With MLL2/H3K4me3 to Upregulate FOXP4

2021 ◽  
Vol 11 ◽  
Author(s):  
Yunfeng Niu ◽  
Gaoyan Wang ◽  
Yan Li ◽  
Wei Guo ◽  
Yanli Guo ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Molecular Mechanism ◽  
Squamous Cell ◽  
Cell Function ◽  
Malignant Tumors ◽  
Luciferase Reporter ◽  
Invasion And Migration ◽  
And Migration

Malignant tumors are a grave threat to human health. Esophageal squamous cell carcinoma (ESCC) is a common gastrointestinal malignant tumor. China has a high incidence of ESCC, and its morbidity and mortality are higher than the global average. Increasingly, studies have shown that long noncoding RNAs (lncRNAs) play a vital function in the occurrence and development of tumors. Although the biological function of FOXP4-AS1 has been demonstrated in various tumors, the potential molecular mechanism of FOXP4-AS1 in ESCC is still poorly understood. The expression of FOXP4 and FOXP4-AS1 was detected in ESCC by quantitative real-time PCR (qRT–PCR) or SP immunohistochemistry (IHC). shRNA was used to silence gene expression. Apoptosis, cell cycle, MTS, colony formation, invasion and migration assays were employed to explore the biological functions of FOXP4 and FOXP4-AS1. The potential molecular mechanism of FOXP4-AS1 in ESCC was determined by dual-luciferase reporter, RNA immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP). Here, we demonstrated that FOXP4-AS1 was significantly increased in ESCC tissues and cell lines, associated with lymph node metastasis and TNM staging. Cell function experiments showed that FOXP4-AS1 promoted the proliferation, invasion and migration ability of ESCC cells. The expression of FOXP4-AS1 and FOXP4 in ESCC tissues was positively correlated. Further research found that FOXP4-AS1, upregulated in ESCC, promotes FOXP4 expression by enriching MLL2 and H3K4me3 in the FOXP4 promoter through a “molecular scaffold”. Moreover, FOXP4, a transcription factor of β-catenin, promotes the transcription of β-catenin and ultimately leads to the malignant progression of ESCC. Finally, FOXP4-AS1 may be a new therapeutic target for ESCC.

scholarly journals Silencing of lncRNA NEAT1 inhibits esophageal squamous cell carcinoma proliferation, migration, and invasion via regulation of the miR-1299/MMP2 axis

2021 ◽  
Author(s):  
Zhanfeng Yang ◽  
Meilin Zhu ◽  
Jingjing Zhang ◽  
Guangchong Zhang ◽  
Jun Hu ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Malignant Tumors ◽  
Matrix Metalloproteinase 2 ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Lncrna Neat1

AbstractEsophageal squamous cell carcinoma (ESCC) is the most prevalent form of esophageal cancer worldwide. Considerable evidence has verified that abnormal expression of lncRNAs can effectively influence the progression of various malignant tumors. However, the regulatory mechanisms of lncRNAs underlying ESCC development and progression remain poorly defined. Here, we investigated the role of lncRNA nuclear-enriched abundant transcript 1 (NEAT1) in ESCC via regulating microRNA 1299 (miR-1299) and matrix metalloproteinase 2 (MMP2). A total of 32 ESCC tissue samples were obtained from the First Affiliated Hospital of Zhengzhou University. The mRNA levels of lncRNA NEAT1, miR-1299, and MMP2 mRNA were measured via quantitative real-time PCR. Interactions among miR-1299, lncRNA NEAT1, and MMP2 mRNA in EC9706 cells were confirmed by dual-luciferase reporter assays and RNA immunoprecipitation (RIP) assays. The proliferation and migration/invasion of ESCC cells were verified by CCK-8 and transwell assays, respectively. lncRNA NEAT1 was up-regulated in ESCC tissues and cells. lncRNA NEAT1 silencing inhibited migration, invasion, and proliferation of ESCC cells. Furthermore, lncRNA NEAT1 sponged and negatively regulated miR-1299, thus giving rise to increased expression of MMP2. Moreover, miR-1299 inhibitors and MMP2 rescued the invasion of ESCC cells following silencing of lncRNA NEAT1. lncRNA NEAT1 was overexpressed in ESCC tissues and cells. Silencing of lncRNA NEAT1 inhibited ESCC proliferation, migration, and invasion via reducing competitive binding of lncRNA NEAT1 with miR-1299 and enhancing miR-1299-targeted suppression of MMP2. Taken together, our findings suggest that lncRNA NEAT1 is a potential target for ESCC therapy and rehabilitation.

Lentiviral-Mediated Overexpression of MicroRNA-141 Promotes Cell Proliferation and Inhibits Apoptosis in Human Esophageal Squamous Cell Carcinoma

2019 ◽  
Vol 14 (2) ◽  
pp. 170-176 ◽  
Author(s):  
Jun-He Zhang ◽  
Hai-Bin Xia
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Tumour Growth ◽  
Direct Interaction ◽  
Vital Role ◽  
Expression Level ◽  
Luciferase Reporter

Background:Esophageal Carcinoma (EC) is the eighth most common cancer worldwide. Numerous studies have highlighted a vital role of microRNAs (miRNAs) in the development of EC. However, the mechanism of microRNA (miRNA)-141 in Esophageal Squamous Cell Carcinoma (ESCC) remains unknown.Objective:In this study, we explored the effects of miRNA-141 on EC cell proliferation, apoptosis, xenograft tumour growth and their possible mechanisms.Methods :A lentivirus-vector-expressing miRNA-141 was constructed, and a TE-1 cell line of ESCC with a stable expression of miRNA-141 was transfected and screened. The miRNA-141 expression level was detected using qRT-PCR. Effects of miRNA-141 overexpression on cell proliferation and apoptosis were detected using MTT and flow cytometry, respectively. Using a dual-luciferase reporter assay, a direct interaction between miRNA-141 and the 3'-Untranslated Region (UTR) of YAP1 and SOX17 was confirmed. Tumour xenograft experiment in nude mice was used to detect the tumour growth, and the effects of miRNA-141 overexpression on YAP1 and SOX17 were analysed using Western blot.Results:We found that miRNA-141 was highly expressed in TE-1 cells, and miRNA-141 overexpression promoted cell proliferation and inhibited apoptosis. Moreover, the miRNA-141 group showed significantly increased tumour growth ability, luciferase activities and expression levels of YAP1 and SOX17 in the miRNA-141group were significantly down-regulated.Conclusion:miRNA-141 promotes cell proliferation and inhibits apoptosis in ESCC by downregulating the expression level of YAP1 and SOX17, indicating that miRNA-141 may be a potential molecular target for the treatment of ESCC.

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