scholarly journals Long Non-Coding RNA LINC00663 Promotes Gliomagenesis and Progression

2020 ◽  
Author(s):  
Meichen Pan ◽  
Jingren Shi ◽  
Shangqi Yin ◽  
Huan Meng ◽  
Chaonan He ◽  
...  
Keyword(s):  
Glioma Cells ◽  
Migration And Invasion ◽  
High Morbidity ◽  
Akt Activation ◽  
In Vivo Experiments ◽  
Dismal Prognosis ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Background: Glioma is the most frequent primary malignant brain tumor, characterized by high morbidity, high mortality and dismal prognosis. Numerous analyses have revealed the abnormal expression of long non-coding RNAs (lncRNAs) in glioma cells. This study aims to explore its role in glioma development and prognosis.Methods: The gene expression in cell lines were measured by qRT-PCR. The role of LINC00663 in glioma was confirmed by CCK8, EdU assay, transwell and western blot as well as by in vivo experiments. Besides, Pearson's correlation analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were also performed as needed.Results: Firstly, data from our preliminary work (NSFC NO. 81572474) showed that LINC00663 might be largely implicated in glioma. Meanwhile, LINC00663 upregulation confirmed in glioma predicted poor clinical outcomes. Functionally, LINC00663 knockdown restrained cell proliferation, migration and invasion in vitro. Mechanistic investigations validated that LINC00663 silencing decreased AKT activation in glioma cells.Conclusions: LINC00663 promotes glioma development and progression through regulating AKT pathway, suggesting LINC00663 as a probable target for glioma treatment.

scholarly journals An in vitro and in vivo study of the role of long non-coding RNA-HOST2 in the proliferation, migration, and invasion of human glioma cells

IUBMB Life ◽  
2018 ◽  
Vol 71 (1) ◽  
pp. 93-104 ◽  
Author(s):  
Qi Wang ◽  
Zhong-Wei Zhuang ◽  
Yi-Ming Cheng ◽  
Ji-Qiang Ma ◽  
Shi-Yi Xu ◽  
...  
Keyword(s):  
Glioma Cells ◽  
In Vivo Study ◽  
Migration And Invasion ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Long Non-Coding RNA ARAP1-AS1 Facilitates the Progression of Cervical Cancer by Regulating miR-149-3p and POU2F2

Pathobiology ◽  
2021 ◽  
pp. 1-12
Author(s):  
Ling Zhou ◽  
Xiao-li Xu
Keyword(s):  
Cervical Cancer ◽  
Tumor Model ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Non Coding Rna ◽  
Injection Model ◽  
Rna Immunoprecipitation ◽  
Long Non Coding Rna

<b><i>Background:</i></b> Emerging research has demonstrated that long non-coding RNAs (lncRNAs) attach great importance to the progression of cervical cancer (CC). LncRNA ARAP1-AS1 was involved in the development of several cancers; however, its role in CC is far from being elucidated. <b><i>Methods:</i></b> Real-time PCR (RT-PCR) was employed to detect ARAP1-AS1 and miR-149-3p expression in CC samples. CC cell lines (HeLa and C33A cells) were regarded as the cell models. The biological effect of ARAP1-AS1 on cancer cells was measured using CCK-8 assay, colony formation assay, flow cytometry, Transwell assay and wound healing assay in vitro, and subcutaneous xenotransplanted tumor model and tail vein injection model in vivo. Furthermore, interactions between ARAP1-AS1 and miR-149-3p, miR-149-3p and POU class 2 homeobox 2 (POU2F2) were determined by bioinformatics analysis, qRT-PCR, Western blot, luciferase reporter and RNA immunoprecipitation assay, respectively. <b><i>Results:</i></b> The expression of ARAP1-AS1 was enhanced in CC samples, while miR-149-3p was markedly suppressed. Additionally, ARAP1-AS1 overexpression enhanced the viability, migration, and invasion of CC cells. ARAP1-AS1 downregulated miR-149-3p via sponging it. ARAP1-AS1 and miR-149-3p exhibited a negative correlation in CC samples. On the other hand, ARAP1-AS1 enhanced the expression of POU2F2, which was validated as a target gene of miR-149-3p. <b><i>Conclusion:</i></b> ARAP1-AS1 was abnormally upregulated in CC tissues and indirectly modulated the POU2F2 expression via reducing miR-149-3p expression. Our study identified a novel axis, ARAP1-AS1/miR-149-3p/POU2F2, in CC tumorigenesis.

scholarly journals Long Non-Coding RNA AC022306.2 Promotes Cell Proliferation, Migration, and Invasion by Mediating GALK2 in Epithelial Ovarian Cancer

2021 ◽  
Author(s):  
Xin Liu ◽  
Zhenghao Huang ◽  
Honglei Qin ◽  
Jingwen Chen ◽  
Yang Zhao
Keyword(s):  
Ovarian Cancer ◽  
Figo Stage ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Reporter System ◽  
Non Coding Rna ◽  
Tumor Tissues ◽  
Long Non Coding Rna

Abstract BackgroundLong non-coding RNA (LncRNA) has been exhibited to exert significant function among human cancers. AC022306.2, as a newly discovered lncRNA, has an unclear function in ovarian cancer (OC). This study aims to uncover the functional role of AC022306.2 in OC and discover its possible mechanism. MethodsThe expression of AC022306.2 and Galactokinase 2 (GALK2) in OC tissues and adjacent non-tumor tissues was detected via qRT-PCR. The CCK-8 assay, cell clonogenesis assay, scratch healing assay and trans-well assay were used to reveal the function of AC022306.2 and GALK2 in ovarian cancer cell lines. Mice xenografts experiment was performed. Bioinformatics predicted the microRNA (miRNA) that bond with AC022306.2 and GALK2, and dual luciferase reporter system confirmed it. Rescue experiments of miRNA mimics and siGALK2 transfection on the basis of AC022306.2 over-expression were carried out to uncover the mechanism by which AC022306.2 played cancer-promoting roles in ovarian cancer.ResultsIt was found that AC022306.2 was up-regulated in EOC tissues compared with adjacent non-tumor tissues. The elevated expression of AC022306.2 was related to the FIGO stage of OC. Functional experiments showed that AC022306.2 overexpression accelerated proliferation and aggression of OC cells in vitro and accelerated tumor growth in vivo. We also found that GALK2 was up-regulated in OC tissues. The expression of GALK2 mRNA in OC tissue was positively associated with the expression of AC022306.2. After AC022306.2 was knocked down, the expression of GALK2 was down-regulated. In addition, GALK2 depletion restored the proliferation and aggression capabilities of OC cells after AC022306.2 overexpression. Mechanically, AC022306.2 acted as a competitive endogenous RNA (ceRNA) of miR-369-3p to modulate the expression of GALK2. The up-regulating of miR-369-3p or the down-regulating of GALK2 partially reversed the effect of AC022306.2 overexpressed on cell propagation and aggression in OC. ConclusionsAC022306.2 is a new oncogene in the carcinogenesis and development of OC. AC022306.2 improves the development of OC by regulating the miR-369-3p / GALK2 axis, indicating that AC022306.2 may have the potential to become a new molecular target for the treatment of OC.

AC006262.5/miR-7855-5p/BPY2C axis facilitates hepatocellular carcinoma proliferation and migration

2020 ◽  
Author(s):  
Fenrong Chen ◽  
Yan Wang ◽  
Yan Cheng ◽  
Haitao Shi ◽  
Hong Li ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Human Life ◽  
Migration And Invasion ◽  
Non Coding Rna ◽  
Novel Targets ◽  
And Migration ◽  
Regulatory Loop ◽  
Long Non Coding Rna

Hepatocellular carcinoma (HCC) is a considerable threat to human life, and patients with HCC are usually diagnosed in the later stages. Although treatment for HCC has recently advanced rapidly, novel targets for HCC are still desperately needed, especially for precision medicine. Here, we identified an HCC enriched long non-coding RNA, AC006262.5, that promoted the proliferation, migration, and invasion of HCC both in vitro and in vivo. In addition, our results revealed that AC006262.5 bound to and regulated miR-7855-5p, a tumor suppressive miRNA in HCC. Moreover, our data illustrated that AC006262.5 regulated the expression of BPY2C via miR-7855-5p. Finally, we found that AC006262.5 and miR-7855-5p formed a regulatory loop. Upregulation of AC006262.5 resulted in the decreased expression of miR-7855-5p, and downregulation of miR-7855-5p further facilitated the expression of AC006262.5. Our study provides novel targets for HCC diagnosis and treatment and sheds light on the lncRNA-miRNA regulatory nexus that controls the pathology of HCC.

scholarly journals Long non-coding RNA LINC01116 is activated by EGR1 and facilitates lung adenocarcinoma oncogenicity via targeting miR-744-5p/CDCA4 axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Ping Ren ◽  
Liang Chang ◽  
Xiaodong Hong ◽  
Lei Xing ◽  
Hong Zhang
Keyword(s):  
Lung Adenocarcinoma ◽  
Biological Effects ◽  
Human Lung Cancer ◽  
Migration And Invasion ◽  
Transcription Activator ◽  
Protein Levels ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract Background Lung adenocarcinoma (LAD) is one of the most frequently diagnosed pathological categories of human lung cancer. Nevertheless, the link between long non-coding RNA (lncRNA) LINC01116 and LAD remains poorly investigated. Methods QRT-PCR and western blot were applied for quantifying the expression of RNAs and proteins. Both functional experiments assays in vitro and xenografts model in vivo were implemented for analyzing LINC01116 function in LAD while molecular relationship among RNAs was investigated via mechanism experiments. Results LINC01116 was expressed at an abnormally high level in LAD, which was induced by transcription activator EGR1. LINC01116 depletion restrained proliferation, migration and invasion, yet facilitated apoptosis of LAD cells. MiR-744-5p could bind to LINC01116. MiR-744-5p inhibitor reversed the inhibitory effects of silencing LINC01116 on LAD malignant behaviors. In addition, cell division cycle-associated protein 4 (CDCA4) shared binding sites with miR-744-5p. Silencing LINC01116 elicited decline in CDCA4 mRNA and protein levels. Moreover, CDCA4 up-regulation could counteract the biological effects of LINC01116 knockdown on LAD cells. Conclusion Our data revealed that LINC01116 promoted malignant behaviors of LAD cells by targeting miR-744-5p/CDCA4 axis, implying the theoretical potential of LINC01116 as a novel target for LAD treatment.

scholarly journals Downregulation of Long Non-Coding RNA Kcnq1ot1: An Important Mechanism of Arsenic Trioxide-Induced Long QT Syndrome

2018 ◽  
Vol 45 (1) ◽  
pp. 192-202 ◽  
Author(s):  
Yanan Jiang ◽  
Weijie Du ◽  
Qun Chu ◽  
Ying Qin ◽  
Gulnara Tuguzbaeva ◽  
...  
Keyword(s):  
Arsenic Trioxide ◽  
Long Qt Syndrome ◽  
Long Qt ◽  
In Vivo Experiments ◽  
Qt Interval Prolongation ◽  
Non Coding Rna ◽  
Qt Syndrome ◽  
Long Non Coding Rna

Background/Aims: Arsenic trioxide (ATO) is a known anti-acute promyelocytic leukemia (APL) reagent, whose clinical applications are limited by its serious cardiac toxicity and fatal adverse effects, such as sudden cardiac death resulting from long QT syndrome (LQTS). The mechanisms of cardiac arrhythmia due to ATO exposure still need to be elucidated. Long non-coding RNAs (lncRNAs) are emerging as major regulators of various pathophysiological processes. This study aimed to explore the involvement of lncRNAs in ATO-induced LQTS in vivo and in vitro. Methods: For in vivo experiments, mice were administered ATO through the tail vein. For in vitro experiments, ATO was added to the culture medium of primary cultured neonatal mouse cardiomyocytes. To evaluate the effect of lncRNA Kcnq1ot1, siRNA and lentivirus-shRNA were synthesized to knockdown lncRNA Kcnq1ot1. Results: After ATO treatment, the Kcnq1ot1 and Kcnq1 expression levels were down regulated. lncRNA Kcnq1ot1 knockdown prolonged the action potential duration (APD) in vitro and exerted LQTS in vivo. Correspondingly, Kcnq1 expression was decreased after silencing lncRNA Kcnq1ot1. However, the knockdown of Kcnq1 exerted no effect on lncRNA Kcnq1ot1 expression. Conclusions: To our knowledge, this report is the first to demonstrate that lncRNA Kcnq1ot1 downregulation is responsible for QT interval prolongation induced by ATO at least partially by repressing Kcnq1 expression. lncRNA Kcnq1ot1 has important pathophysiological functions in the heart and could become a novel antiarrhythmic target.

scholarly journals Long non-coding RNA PSMA3-AS1 enhances cell proliferation, migration and invasion by regulating miR-302a-3p/RAB22A in glioma

2020 ◽  
Vol 40 (9) ◽  
Author(s):  
Li-li Zhou ◽  
Meng Zhang ◽  
Yan-zhen Zhang ◽  
Mei-fen Sun
Keyword(s):  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Nude Mouse Model ◽  
Cell Behaviors ◽  
Non Coding Rna ◽  
The Central Nervous System ◽  
Long Non Coding Rna

Abstract Glioma is the most prevalent solid tumor in the central nervous system (CNS). Recently, it has been indicated that long non-coding RNAs (lncRNAs) substantially adjust the development of a variety of human cancers. In the present study, it was found and verified via microarray analysis that lncRNA PSMA3-AS1 exhibited a high expression in glioma tissues and cell lines. Then CCK-8, 5-Ethynyl-2′-deoxyuridine (EdU) staining, plate clone assay, Transwell assay, Western blotting and nude mouse model were adopted to verify PSMA3-AS1’s effects on glioma. Knockdown of PSMA3-AS1 inhibited the migration, proliferation and invasion of glioma cells in vivo and in vitro. Besides, PSMA3-AS1 bound to miR-302a-3p directly reduced the expression of miR-302a-3p, thus functioning as an endogenous sponge confirmed by luciferase reporter assay and bioinformatics analysis. PSMA3-AS1 knockdown remarkably enhanced the role of miR-302a-3p overexpression in cell behaviors in glioma. Moreover, these assays also confirmed that RAB22A was a target of miR-302a-3p. In this research, therefore, the PSMA3-AS1/miR-302a-3p/RAB22A pathway regulatory axis may be revealed in the pathogenesis of glioma, and PSMA3-AS1 can be used as an underlying target for the treatment and prognosis of glioma.

scholarly journals The long non-coding RNA HOXA11-AS activates ITGB3 expression to promote the migration and invasion of gastric cancer by sponging miR-124-3p

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Liting You ◽  
Qian Wu ◽  
Zhaodan Xin ◽  
Huiyu Zhong ◽  
Juan Zhou ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Non Coding Rna ◽  
And Function ◽  
Long Non Coding Rna ◽  
Invasion Assays

Abstract Background miR-124-3p can inhibit integrin β3 (ITGB3) expression to suppress the migration and invasion of gastric cancer (GC), and in the process lncRNA HOXA11-AS may act as a molecular sponge. Methods Luciferase reporter assay was conducted to verify the binding of miR-124-3p and HOXA11-AS. RT-PCR and western blot were performed to detect the expression of HOXA11-AS, miR-124-3p and ITGB3 in GC tissues and cells. Gene silence and overexpression experiments as well as cell migration and invasion assays on GC cell lines were performed to determine the regulation of molecular pathways, HOXA11-AS/miR-124-3p/ITGB3. Furthermore, the role of HOXA11-AS in GC was confirmed in mice models. Results We found HOXA11-AS is up-regulated in GC tissues and can bind with miR-124-3p. Through overexpression/knockdown experiments and function tests in vitro, we demonstrated HOXA11-AS can promote ITGB3 expression by sponging miR-124-3p, consequently enhance the proliferation, migration, and invasion of GC cells. Meanwhile, we validated that HOXA11-AS promotes migration and invasion of GC cells via down-regulating miR-124-3p and up-regulating ITGB3 in vivo. Conclusions We demonstrated that lncRNA HOXA11-AS can increase ITGB3 expression to promote the migration and invasion of gastric cancer by sponging miR-124-3p. Our results suggested that HOXA11-AS may reasonably serve as a promising diagnostic biomarker and a potential therapeutic target of GC.

scholarly journals Long non-coding RNA H19 promotes colorectal cancer metastasis via binding to hnRNPAA2B1

2020 ◽  
Author(s):  
Yu-Hui Zhang ◽  
Wei-Bin Huang ◽  
Yu-Jie Yuan ◽  
Jin Li ◽  
Jing Wu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Metastasis ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Qrt Pcr ◽  
Non Coding Rna ◽  
Potential Biomarker ◽  
Long Non Coding Rna

Abstract Background Long non-coding RNA H19 was demonstrated to be significantly correlated with tumor metastasis. However, the specific functions of H19 in colorectal cancer (CRC) metastasis and the underlying mechanism are still largely unclear. Methods Use public database to screen the potential lncRNA crucial for metastasis in colorectal cancer. The expression of H19 in clinical CRC specimens was detected by qRT-PCR. The effect of H19 on the metastasis of CRC cells was investigated by transwell, wound healing assays, CCK-8 assays and animal studies. The potential proteins binding to H19 was identified by LC-MS and verified by RNA immunoprecipitation (RIP). The expression of indicated RNA and proteins were measured by qRT-PCR or western blot. Results We found the expression of lncRNA H19 was significantly upregulated in primary tumor and metastatic tissues, correlated with poor prognosis in CRC. Ectopic H19 expression promoted the metastasis of colorectal cancer cells in vitro and in vivo , and induced epithelial-to-mesenchymal transition (EMT). Mechanistically, H19 directly bound to hnRNPA2B1. Knockdown of hnRNPA2B1 attenuated the H19-induce migration and invasion in CRC cells. Furthermore, H19 stabilized and upregulated the expression of Raf-1 by facilitated the interaction between hnRNPA2B1 and Raf-1 mRNA, resulting in activation of Raf-ERK signaling. Conclusions Our findings demonstrate the role of H19/hnRNPA2B1/EMT axis in regulation CRC metastasis, suggested H19 could be a potential biomarker to predict prognosis as well as a therapeutic strategy for CRC.

scholarly journals Long non-coding RNA SNHG3 promotes progression of gastric cancer by regulating neighboring MED18 gene methylation

2019 ◽  
Vol 10 (10) ◽  
Author(s):  
Yi Xuan ◽  
Yanong Wang
Keyword(s):  
Gastric Cancer ◽  
Migration And Invasion ◽  
Gene Methylation ◽  
Free Survival ◽  
Non Coding Rna ◽  
Ectopic Overexpression ◽  
Potential Impact ◽  
Long Non Coding Rna

Abstract To understand the mechanistic involvement of long non-coding RNA (lncRNA) SNHG3 in gastric cancer (GC), the relative abundance of SNHG3 was determined by real-time PCR. Overall and metastasis-free survival was analyzed by Kaplan–Meier’s plot. The potential impact of SNHG3 on tumor progression was evaluated both in vitro and in vivo. The in vivo metastasis was monitored in the tail vein-injected mice. Our data suggested that high SNHG3 associated with unfavorable prognosis in respect to overall and metastasis-free survival. SNHG3-deficiency significantly suppressed cell proliferation and cell viability in vitro and xenograft progression in vivo. In addition, ectopic overexpression of SNHG3 promoted cell migration and invasion in vitro and lung metastasis in vivo. Mechanistically, we uncovered SNHG3 associated with EZH2 and negatively regulated MED18 expression through methylation modulation. Transient knockdown of MED18 in SNHG3-deficient cells completely rescued the tumor suppressive phenotypes in GC cells. Our data unraveled the oncogenic properties of high SNHG3 in GC, which predominantly depended on epigenetically regulated MED18.

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