scholarly journals Polysome profiling followed by quantitative PCR for identifying potential micropeptide encoding long non-coding RNAs in suspension cell lines

2022 ◽  
Vol 3 (1) ◽  
pp. 101037
Author(s):  
Cai Han ◽  
Linyu Sun ◽  
Qi Pan ◽  
Yumeng Sun ◽  
Wentao Wang ◽  
...  
Keyword(s):  
Quantitative Pcr ◽  
Cell Lines ◽  
Suspension Cell ◽  
Polysome Profiling ◽  
Non Coding Rnas

lncLocator 2.0: a cell-line-specific subcellular localization predictor for long non-coding RNAs with interpretable deep learning

2021 ◽  
Author(s):  
Yang Lin ◽  
Xiaoyong Pan ◽  
Hong-Bin Shen
Keyword(s):  
Subcellular Localization ◽  
Cell Line ◽  
Cell Lines ◽  
Short Term Memory ◽  
Computational Method ◽  
Language Models ◽  
Supplementary Information ◽  
Deep Model ◽  
A Cell ◽  
Non Coding Rnas

Abstract Motivation Long non-coding RNAs (lncRNAs) are generally expressed in a tissue-specific way, and subcellular localizations of lncRNAs depend on the tissues or cell lines that they are expressed. Previous computational methods for predicting subcellular localizations of lncRNAs do not take this characteristic into account, they train a unified machine learning model for pooled lncRNAs from all available cell lines. It is of importance to develop a cell-line-specific computational method to predict lncRNA locations in different cell lines. Results In this study, we present an updated cell-line-specific predictor lncLocator 2.0, which trains an end-to-end deep model per cell line, for predicting lncRNA subcellular localization from sequences.We first construct benchmark datasets of lncRNA subcellular localizations for 15 cell lines. Then we learn word embeddings using natural language models, and these learned embeddings are fed into convolutional neural network, long short-term memory and multilayer perceptron to classify subcellular localizations. lncLocator 2.0 achieves varying effectiveness for different cell lines and demonstrates the necessity of training cell-line-specific models. Furthermore, we adopt Integrated Gradients to explain the proposed model in lncLocator 2.0, and find some potential patterns that determine the subcellular localizations of lncRNAs, suggesting that the subcellular localization of lncRNAs is linked to some specific nucleotides. Availability The lncLocator 2.0 is available at www.csbio.sjtu.edu.cn/bioinf/lncLocator2 and the source code can be found at https://github.com/Yang-J-LIN/lncLocator2. Supplementary information Supplementary data are available at Bioinformatics online.

scholarly journals Gene expression variability between randomly and targeted transgene integration events in tobacco suspension cell lines

2020 ◽  
Vol 14 (4) ◽  
pp. 451-458
Author(s):  
Janina Kirchhoff ◽  
Andreas Schiermeyer ◽  
Katja Schneider ◽  
Rainer Fischer ◽  
W. Michael Ainley ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Lines ◽  
Suspension Cell ◽  
Expression Variability ◽  
Transgene Integration ◽  
Tobacco Suspension Cell

scholarly journals Long Non-Coding RNA Linc-USP16 Functions As a Tumour Suppressor in Hepatocellular Carcinoma by Regulating PTEN Expression

2017 ◽  
Vol 44 (3) ◽  
pp. 1188-1198 ◽  
Author(s):  
Jidong Sui ◽  
Xuejun Yang ◽  
Wenjing Qi ◽  
Kun Guo ◽  
Zhenming Gao ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Lines ◽  
Tumour Suppressor ◽  
Pten Expression ◽  
The Novel ◽  
Aberrant Expression ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
And Migration ◽  
Long Non Coding Rna

Background/Aims: Recent evidence has indicated the crucial regulatory roles of long non-coding RNAs (lncRNAs) in tumour biology. In hepatocellular carcinoma (HCC), aberrant expression of lncRNAs plays an essential role in HCC tumourigenesis. However, the potential roles and regulatory mechanisms of the novel human lncRNA, Linc-USP16, in HCC are unclear. Methods: To investigate the function of Linc-USP16 in HCC, we first analysed the expression levels of Linc-USP16 in HCC patient tissues and cell lines via q-RT-PCR and established overexpressed or knockdown HCC cell lines. Results: Here, we found that Linc-USP16 expression was significantly down-regulated in HCC patient tissues and cell lines. Further functional experiments suggested that Linc-USP16 could directly increase PTEN expression by acting as a competing endogenous RNA (ceRNA) for miR-21 and miR-590-5p. These interactions led to repression of AKT pathway and inhibition of HCC cell proliferation and migration. Conclusion: Thus, our data showed that Linc-USP16, as a tumour suppressor, plays an important role in HCC pathogenesis and provides a new therapeutic strategy for HCC treatment.

scholarly journals RPS27A is a Poor Prognostic Predictor for Hepatocellular Carcinoma via Interacting with METTL3-Mediated RNA Modifications

2021 ◽  
Author(s):  
Huiying Liu ◽  
Jianjun Zhu ◽  
Xiaoxia Kou ◽  
Lingling Guo ◽  
Hongjuan Zhang ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Quantitative Pcr ◽  
Cell Lines ◽  
Disease Free Survival ◽  
Rna Modification ◽  
Ppi Network ◽  
Rna Modifications ◽  
Pcr Assay ◽  
Prognostic Predictor ◽  
Quantitative Pcr Assay

Abstract Background: Increasing evidence has pointed to the involvement of RNA modifications in the pathogenesis of human cancers. However, they are rarely studied in hepatocellular carcinoma (HCC). Method: We summarized multiple types of RNA modification-related genes (RMRGs) from public references, and identified differentially expressed RMRGs (DEGs) between HCC tissues and matched normal samples, where their genetic variation were then investigated. The potential hub genes in the protein-protein interaction (PPI) network constructed by co-expression genes of RMRGs were recognized and verified in METTL3-knockdown HCC cell lines by quantitative PCR assay.Results: Seventy-six RMRGs, including six writers, seven readers, and seven erasers, were collected, of which 34 were identified and validated as DEGs. YTHDC2 exhibited the highest mutation rate, while ADAT2 showed widespread deletions. High correlations were observed between the expressions of 34 RMRGs. The PPI network constructed by 1080 co-expression DEGs related to RNA regulations consisted of 513 nodes and 11557 edges, with RPS27A presented the most directed edges and maximum closeness centrality. Patients with high expression of RPS27A showed worse overall survival (P < 0.01) and disease-free survival (P = 0.019). Moreover, RPS27A was found upregulated on high-risk metastatic and recurrent HCC tissues. Quantitative PCR assay indicated that RPS27A was significantly decreased in cancer cell lines when METTL3 was knocked down. Conclusions: Remarkable differences were observed for RNA modifications between HCC and normal samples, and RPS27A could be a poor prognostic predictor for HCC via interacting with METTL3-mediated RNA modifications.

scholarly journals LncRNA LINC01518 induced by GATA3 promotes cell proliferation, migration and invasion via miR-206/PRKACB in neuroblastoma

2021 ◽  
Author(s):  
Chunying Zhang ◽  
Lin Yang ◽  
Ge Zhao ◽  
Jiaxiang Wang ◽  
Juntao Pan ◽  
...  
Keyword(s):  
Cell Lines ◽  
Migration And Invasion ◽  
Cell Phenotype ◽  
Competing Endogenous Rna ◽  
Protein Coding ◽  
Solid Malignancy ◽  
Active Transcription ◽  
Non Coding Rnas ◽  
Regulate Protein

Neuroblastoma (NBL) exists as the most common solid malignancy which predominantly occurs in children. Long non-coding RNAs (lncRNAs) have been widely confirmed to exert functions in modulating the pathogenesis of diverse diseases. Nevertheless, whether the putative function of long intergenic non-protein coding RNA 1518 (LINC01518) in NBL has not been elucidated yet. In this study, RT-qPCR was used for determining LINC01518 expression and LINC01518 was found to be notably overexpressed in NBL tissues and cell lines compared with normal nerve tissues and cell lines. Functional experiments and mechanism assays were respectively done for the investigation into cell phenotype and for the exploration of correlation among genes. LINC01518 silencing was discovered to repress cell malignant phenotype. We observed that GATA binding protein 3 (GATA3) was an active transcription factor of LINC01518. Besides, LINC01518 functioned as a competing endogenous RNA (ceRNA), which sequestered microRNA-206 (miR-206) to up-regulate protein kinase cAMP-activated catalytic subunit beta (PRKACB). Afterwards, rescue assays validated the oncogenic role of GATA3/LINC01518/miR-206/PRKACB axis in NBL. To be summarized, our research determined that LINC01518 might be used as a putative molecular marker for NBL diagnosis and treatment.

scholarly journals MicroRNA-367 directly targets PIK3R3 to inhibit proliferation and invasion of oral carcinoma cells

2020 ◽  
Vol 40 (5) ◽  
Author(s):  
Haitao Sun ◽  
Xiaodong Feng
Keyword(s):  
Quantitative Pcr ◽  
Cell Lines ◽  
Hepatocellular Cancer ◽  
Carcinoma Cells ◽  
Luciferase Reporter ◽  
Pcr Assay ◽  
Protein Levels ◽  
Cancer Types ◽  
Proliferation And Invasion ◽  
Quantitative Pcr Assay

Abstract Recently, microRNA-367 (miR-367) has been reported to function as both tumor suppressor and oncogene in several cancer types, including gastric cancer, hepatocellular cancer and lung cancer. However, the biological function of miR-367 and its precise mechanisms in oral squamous cell carcinoma (OSCC) have not been well clarified. The aim of the present study was to study the roles of miR-367/PIK3R3 axis in OSCC. The levels of PIK3R3 and miR-367 were detected by quantitative PCR assay in OSCC tissues and cell lines. Moreover, the biological roles of miR-367 and PIK3R3 in OSCC cells were assessed by cell proliferation and invasion. The mRNA and protein levels of PIK3R3 were determined by using quantitative PCR and Western blotting assays. Luciferase assays were used to confirm that PIK3R3 was one target of miR-367. In the present study, the miR-367 level was dramatically reduced in OSCC tissues and cell lines, and the PIK3R3 expression was significantly enhanced. What’s more, the PIK3R3 expression was negatively related to the miR-367 level in OSCC tissues. Furthermore, up-regulation of miR-367 obviously restrained OSCC cells proliferation and invasion. We confirmed that miR-367 could directly target PIK3R3 by luciferase reporter assay. Besides, knockdown of PIK3R3 also could markedly inhibit the proliferation and invasion of OSCC cells. Finally, overexpression of miR-367 in OSCC cells partially reversed the promoted effects of PIK3R3 up-regulation. Overexpression of miR-367 restrained OSCC cells proliferation and invasion via regulation of PIK3R3.

scholarly journals LncRNA TP73-AS1 down-regulates miR-139-3p to promote retinoblastoma cell proliferation

2019 ◽  
Vol 39 (5) ◽  
Author(s):  
Zhaoxia Xia ◽  
Xiaoxi Yang ◽  
Shuduan Wu ◽  
Zhizhen Feng ◽  
Lei Qu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Migration ◽  
Cell Lines ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Retinoblastoma Cell ◽  
Non Coding Rnas ◽  
In Cells

Abstract Our study aimed to investigate the role of long non-coding RNAs (lncRNA) TP73-AS1 in retinoblastoma (Rb). In the present study, we found that TP73-AS1 was up-regulated, while miR-139–3p was down-regulated in Rb. TP73-AS1 and miR-139-3p were inversely correlated in Rb tissues. In cells of Rb cell lines, overexpression of miR-139-3p failed to affect TP73-AS1, while TP73-AS1 overexpression caused the down-regulated miR-139-3p. TP73-AS1 overexpression caused promoted proliferation of Rb cells but showed no significant effects on cell migration and invasion. miR-139-3p overexpression played an opposite role and attenuated the effects of TP73-AS1 overexpression. Therefore, lncRNA TP73-AS1 may down-regulate miR-139-3p to promote Rb cell proliferation.

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