scholarly journals Retraction of: Long Non-Coding RNA LINC01260 Inhibits the Proliferation, Migration and Invasion of Spinal Cord Glioma Cells by Targeting CARD11 Via the NF-κB Signaling Pathway

2021 ◽  
Vol 55 (5) ◽  
pp. 672-672
Keyword(s):  
Spinal Cord ◽  
Signaling Pathway ◽  
Glioma Cells ◽  
Migration And Invasion ◽  
Non Coding Rna ◽  
Spinal Cord Glioma ◽  
Long Non Coding Rna

scholarly journals Long Non-Coding RNA LINC01260 Inhibits the Proliferation, Migration and Invasion of Spinal Cord Glioma Cells by Targeting CARD11 Via the NF-κB Signaling Pathway

2018 ◽  
Vol 48 (4) ◽  
pp. 1563-1578 ◽  
Author(s):  
Dong-Mei Wu ◽  
Xin-Rui Han ◽  
Xin Wen ◽  
Shan Wang ◽  
Yong-Jian Wang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Target Gene ◽  
Glioma Cells ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Normal Tissues ◽  
Non Coding Rna ◽  
Spinal Cord Glioma ◽  
And Migration ◽  
Long Non Coding Rna

Background/Aims: Spinal cord glioma is a highly aggressive malignancy that commonly results in high mortality due to metastasis, high recurrence and limited treatment regimens. This study aims to elucidate the effects of long non-coding RNA LINC01260 (LINC01260) on the proliferation, migration and invasion of spinal cord glioma cells by targeting Caspase recruitment domain family, member 11 (CARD11) via nuclear factor kappa B (NF-κB) signaling. Methods: The Multi Experiment Matrix (MEM) website was used for target gene prediction, and the DAVID database was used for analysis of the relationship between CARD11 and the NF-κB pathway. In total, 60 cases of glioma tissues and adjacent normal tissues were collected. Human U251 glioma cells were grouped into blank, negative control (NC), LINC01260 vector, CARD11 vector, siRNA-LINC01260, siRNA-CARD11, LINC01260 vector + CARD11 vector and LINC01260 + siRNA-CARD11 groups. A dual-luciferase reporter assay was conducted to verify the target relationship between LINC01260 and CARD11. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot analysis were employed to assess expression of LINC01260, E-cadherin, p53, CARD11, Ki67, N-cadherin, matrix metalloproteinase (MMP)-9, NF-κBp65 and NF-κBp50. MTT, flow cytometry, wound-healing and Transwell assays were performed to examine cell viability, the cell cycle, apoptosis, invasion and migration. Tumor growth was assessed through xenografts in nude mice. Results: CARD11 was confirmed to be a target gene of LINC01260 and was found to be involved in regulating the NF-κB pathway. Compared with adjacent normal tissues, glioma tissues showed reduced expression of LINC01260 and elevated expression of CARD11 and genes related to apoptosis, invasion and migration; activation of NF-κB signaling was also observed. In contrast to the blank and NC groups, an elevated number of cells arrested in G1 phase, increased apoptosis and reduced cell proliferation, invasion and number of cells arrested in S and G2 phases, as well as tumor growth were found for the LINC01260 vector and siRNA-CARD11 groups. Conclusions: Our findings demonstrate that overexpression of LINC01260 inhibits spinal cord glioma cell proliferation, migration and invasion by targeting CARD11 via NF-κB signaling suppression.

scholarly journals Long non-coding RNA HULC regulates growth and metastasis of human glioma cells via induction of apoptosis and inhibits cell migration and invasion

2020 ◽  
Author(s):  
Junfeng Ma ◽  
Liang Zhou
Keyword(s):  
Cancer Cells ◽  
Signaling Pathway ◽  
Glioma Cells ◽  
Akt Signaling ◽  
Cell Counting ◽  
Migration And Invasion ◽  
Human Glioma ◽  
Akt Signaling Pathway ◽  
Non Coding Rna ◽  
Long Non Coding Rna

IntroductionThe long non-coding RNA HULC has been shown to be involved in the development of several human cancers. The present study was undertaken to investigate the regulatory role of lncRNA-HULC in growth and metastasis of human glioma.Material and methodsThe gene expression of lncRNA-HULC was estimated from the clinical glioma tissues and cell lines using RT-PCR. The proliferation of transfected cancer cells was determined with the help of cell counting kit-8 (CCK8). DAPI staining and dual annexin V-FITC/PI staining procedures were used for inferring the apoptosis of transfected cancer cells. Scratch-heal and transwell chamber assays were employed for the determination of migration and invasion of transfected cells. The expression of proteins of interest was studied by western blotting technique.ResultsThe results showed that lncRNA-HULC exhibits significantly (p < 0.05) higher expression in glioma tissues and cancer cells. The knockdown of lncRNA-HULC led to a marked decline in the proliferation of glioma cells through apoptotic induction which was accompanied by upregulation of Bax and downregulation of Bcl-2. Moreover, knockdown of lncRNA-HULC significantly (p < 0.05) suppressed the migration and invasion of cancer cells in vitro. The western blot analysis showed that lncRNA-HULC exerted its effects via modulation of the PI3K/AKT signaling pathway.ConclusionsThe study revealed the possibility of targeting the PI3K/AKT signaling pathway in glioma through transcriptional knockdown of lncRNA-HULC, which might be utilized for therapeutic purposes against human glioma.

scholarly journals Long non-coding RNA FOXD2-AS1 promotes cell proliferation, metastasis and EMT in glioma by sponging miR-506-5p

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 921-931
Author(s):  
Juan Zhao ◽  
Xue-Bin Zeng ◽  
Hong-Yan Zhang ◽  
Jie-Wei Xiang ◽  
Yu-Song Liu
Keyword(s):  
Cell Proliferation ◽  
Epithelial Mesenchymal Transition ◽  
Human Cancer ◽  
Glioma Cells ◽  
Suppressor Gene ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Non Coding Rna ◽  
Long Non Coding Rna

AbstractLong non-coding RNA forkhead box D2 adjacent opposite strand RNA 1 (FOXD2-AS1) has emerged as a potential oncogene in several tumors. However, its biological function and potential regulatory mechanism in glioma have not been fully investigated to date. In the present study, RT-qPCR was conducted to detect the levels of FOXD2-AS1 and microRNA (miR)-506-5p, and western blot assays were performed to measure the expression of CDK2, cyclinE1, P21, matrix metalloproteinase (MMP)7, MMP9, N-cadherin, E-cadherin and vimentin in glioma cells. A luciferase reporter assay was performed to verify the direct targeting of miR-506-5p by FOXD2-AS1. Subsequently, cell viability was analyzed using the CCK-8 assay. Cell migration and invasion were analyzed using Transwell and wound healing assays, respectively. The results demonstrated that FOXD2-AS1 was significantly overexpressed in glioma cells, particularly in U251 cells. Knockdown of FOXD2-AS1 in glioma cells significantly inhibited cell proliferation, migration, invasion and epithelial–mesenchymal transition (EMT) and regulated the expression of CDK2, cyclinE1, P21, MMP7 and MMP9. Next, a possible mechanism for these results was explored, and it was observed that FOXD2-AS1 binds to and negatively regulates miR-506-5p, which is known to be a tumor-suppressor gene in certain human cancer types. Furthermore, overexpression of miR-506-5p significantly inhibited cell proliferation, migration, invasion and EMT, and these effects could be reversed by transfecting FOXD2-AS1 into the cells. In conclusion, our data suggested that FOXD2-AS1 contributed to glioma proliferation, metastasis and EMT via competitively binding to miR-506-5p. FOXD2-AS1 may be a promising target for therapy in patients with glioma.

scholarly journals The Long Non-Coding RNA CRNDE Promotes Colorectal Carcinoma Progression by Competitively Binding miR-217 with TCF7L2 and Enhancing the Wnt/β-Catenin Signaling Pathway

2017 ◽  
Vol 41 (6) ◽  
pp. 2489-2502 ◽  
Author(s):  
Bo Yu ◽  
Xuan Ye ◽  
Qiong Du ◽  
Bin Zhu ◽  
Qing Zhai
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Western Blotting ◽  
Migration And Invasion ◽  
Down Regulation ◽  
Over Expression ◽  
Non Coding Rna ◽  
Colorectal Cancer Cells ◽  
Long Non Coding Rna

Background/Aims: The long non-coding RNA colorectal neoplasia differentially expressed (CRNDE) contributes to the proliferation and migration of tumors. However, its molecular mechanism underlying gastric cancer remains unknown. In the present study, we investigated whether CRNDE was involved in the development of colorectal cancer via the binding of microRNA (miR)-217 with transcription factor 7-like 2 (TCF7L2) to enhance the Wnt signaling pathway. Methods: Quantitative polymerase chain reaction was used to detect CRNDE, miR-217 and TCF7L2 in colorectal cancer tissues and cells. The CCK-8 assay, wound healing assay, and Transwell assay were used to detect cell proliferation, migration and invasion, respectively. Western blotting and luciferase activity assays were used to identify CRNDE and TCF7L2 as one of the direct targets of miR-217. The activity of the Wnt/β-catenin signaling pathway was analyzed by the TOPflash assay, and the subcellular localization of β-catenin and TCF7L2 was analyzed by western blotting and confocal microscopy. Results: In this study, we found that high expression of CRNDE is negatively correlated with low expression of miR-217 in colorectal cancer tissue and colorectal cancer cells. The dual luciferase reporter analysis showed that miR-217 is bound to CRNDE and TCF7L2 and negatively regulate their expression. CRNDE down-regulation inhibited the cell proliferation, migration and invasion in vitro and in vivo and the inhibitions were both completely blocked after miR-217 inhibition or TCF7L2 overexpression. Finally, TOPflash analysis showed that the activity of Wnt/β-catenin signaling is inhibited by CRNDE down-regulation and rescued by TCF7L2 over-expression. Consistently immunostaining and western blotting analysis showed that the expression of b-catenin and TCF7L2 in the nucleus was significantly decreased by CRNDE down-regulation and was rescued by TCF7L2 over-expression. Conclusions: The present study suggest that CRNDE involves in the cell proliferation, migration and invasion of colorectal cancer cells via increasing the expression of TCF7L2 and activity of Wnt/β-catenin signaling through binding miR-217 competitively.

scholarly journals Long non-coding RNA PVT1 indicates a poor prognosis of glioma and promotes cell proliferation and invasion via target EZH2

2017 ◽  
Vol 37 (6) ◽  
Author(s):  
Anqiang Yang ◽  
Handong Wang ◽  
Xiaobing Yang
Keyword(s):  
Cell Lines ◽  
Molecular Mechanisms ◽  
Malignant Tumors ◽  
Glioma Cells ◽  
Migration And Invasion ◽  
Human Glioma ◽  
Expression Levels ◽  
Non Coding Rna ◽  
Long Non Coding Rna ◽  
Proliferation And Invasion

Human glioma is one of the malignant tumors of the central nervous system (CNS). Its prognosis is poor, which is due to its genetic heterogeneity and our poor understanding of its underlying molecular mechanisms. The present study aimed to assess the relationship between plasmacytoma variant translocation 1 (PVT1) and enhancer of zeste homolog 2 (EZH2), and their effects on the proliferation and invasion of glioma cells. The expression levels of PVT1 and EZH2 in human glioma tissues and cell lines were measured using quantitative RT-PCR (qRT-PCR). Then, after siRNA-PVT1 and entire PVT1 sequence vector transfection, we determined the regulation roles of PVT1 in the proliferation, apoptosis, migration, and invasion of glioma cells. We found that the expression levels of both PVT1 and EZH2 were up-regulated in human glioma tissues and cell lines, and positively correlated with glioma malignancy. And, silencing of PVT1 expression resulted in decreased proliferation, increased apoptosis, and decreased migration and invasion. In addition, exogenous PVT1 led to increased EZH2 expression and increased proliferation and induced proliferation and invasion. These data inferred that long non-coding RNA PVT1 could be served as an indicator of glioma prognosis, and PVT1–EZH2 regulatory pathway may be a novel therapeutic target for treating glioma.

scholarly journals Long non-coding RNA HAL suppresses the migration and invasion of serous ovarian cancer by inhibiting EMT signaling pathway

2020 ◽  
Vol 40 (3) ◽  
Author(s):  
Ke Wu ◽  
Lei Li ◽  
Lin Li ◽  
Dong Wang
Keyword(s):  
Ovarian Cancer ◽  
Signaling Pathway ◽  
Migration And Invasion ◽  
Serous Ovarian Cancer ◽  
Mice Model ◽  
Protein Levels ◽  
Non Coding Rna ◽  
Skov3 Cells ◽  
Long Non Coding Rna

Abstract Objective: To investigate the specific function of long non-coding RNA HAL in serous ovarian cancer (SOC) and to further clarify the regulation of HAL on EMT pathway. Materials and methods: The expression of HAL and TWIST1 was detected by qRT-PCR. CCK8 assay, wound healing assay, transwell assay and flow cytometry were used to detect the HAL function on proliferation, migration, invasion and apoptosis in SOC cells. Western blot was used to calculate protein level of Vimentin, N-cadherin and E-cadherin. The effect of HAL on tumorigenesis of SOC was confirmed by xenograft nude mice model. Results: HAL was significantly decreased in SOC tissues and cells. Overexpression of HAL inhibited the proliferation, migration and invasion of SKOV3 cells, but promoted apoptosis. Furthermore, overexpression of HAL decreased the mRNA and protein levels of TWIST1 via a binding between HAL and TWIST1. Forced expression of TWIST1 reversed the inhibitory role of HAL on SOC cells’ migration and invasion. The in vivo tumor growth assay showed that HAL suppressed SOC tumorigenesis with inhibiting EMT pathway. Conclusions: Our research emphasized HAL acting as a tumor-inhibiting gene by regulating EMT signaling pathway, thus providing some novel experimental basis for clinical treatment of SOC.

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