Non-coding RNA LINC00473 mediates decidualization of human endometrial stromal cells in response to cAMP signaling

Liang, Xiao-Huan; Deng, Wenbo; Liu, Yue-Fang; Liang, Yu‐Xiang; Fan, Zong-Min; Gu, Xu; Liu, Ji‐Long; Sha, Aihua; Diao, Honglu; Yang, Zeng‐Ming

doi:10.1038/srep22744

Cited by 51 publications

(45 citation statements)

References 32 publications

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“…Furthermore, many lines of evidence proved that the PKA pathway might be involved in the up-regulation of lncRNA HULC in liver cancer [23]. Similarly, it has been demonstrated that lncRNA LINC473 expression is highly activated in human decidualization by the cAMP signaling pathway [24], which was also indicated in the present study, in the form of demonstrating the effect of lncRNA LINC01121 on the activation of the cAMP/PKA pathway.…”

Section: Discussionsupporting

confidence: 84%

LINC01121 Inhibits Cell Apoptosis While Facilitating Proliferation, Migration, and Invasion Though Negative Regulation of the Camp/PKA Signaling Pathway via GLP1R

Qian¹,

Zhou²,

Chen³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Pancreatic cancer is an aggressive malignancy as a result of highly metastatic potential. The current study was carried out to alter the expression of LINC01121 in pancreatic cancer, with the aim of elucidating its effects on the biological processes of cell proliferation, migration, invasion, and apoptosis. We hypothesized that both the GLP1R gene and cAMP/PKA signaling pathway participate in the aforementioned process. Methods: Microarray data (GSE14245, GSE27890 and GSE16515) and annotating probe files linked to pancreatic cancer were downloaded through the GEO database. The Multi Experiment Matrix (MEM) site was used to predict the target gene of lncRNA. Both pancreatic cancer tissues (n = 56) and paracancerous tissues (n = 45) were collected from patients diagnosed with pancreatic cancer. Immunohistochemistry was applied to identify the positive expression rate of GLP1R protein. Isolated pancreatic cancer cells and PANC-1 cells were independently classified into the blank, negative control (NC), LINC01121 vector, siRNA-LINC01121, siRNA-GLP1R and siRNA-LINC01121 + siRNA-GLP1R groups. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot analysis were applied to detect the expressions of LINC01121, GLP1R, cAMP, PKA, CREB, Bcl-2, Bad and PCNA. Cell proliferation, migration, invasion, cycle progression, and apoptosis were examined by MTT assay, scratch test, Transwell assay and flow cytometry analyses of Annexin V-FITC/PI staining. Results: Observations were made indicating that LINC01121 was highly expressed, while low expressions of GLP1R in pancreatic cancer were detected based on microarray data, which was largely in consistent with the data collected of LINC01121 and GLP1R within the tissues. The target prediction program and luciferase activity analysis was testament to the notion suggesting that GLP1R was indeed a target of LINC01121. In contrast to the blank and NC groups, the LINC01121 vector group exhibited increased expressions of LINC01121; decreased mRNA and protein levels of GLP1R, Bad, cAMP, and PKA; increased protein levels of CREB, Bcl-2, PCNA, p-PKA and p-CREB; increased cell proliferation, migration and invasion; and decreased cell apoptosis. There was no significant difference detected among the blank, NC, and siRNA-LINC01121 + siRNA-GLP1R groups, except that decreased LINC01121 expression was determined in the siRNA-LINC01121 + siRNA-GLP1R group. Parallel data were observed in the pancreatic cancer cells and PANC-1 cells. Conclusion: The current study presents evidence indicating that LINC01121 might inhibit apoptosis while acting to promote proliferation, migration, and invasion of pancreatic cancer cells, supplementing the stance held that LINC01121 functions as a tumor promoter by means of its involvement in the process of translational repression of the GLP1R and inhibition of the cAMP/PKA signaling pathway.

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Section: Discussionsupporting

confidence: 84%

LINC01121 Inhibits Cell Apoptosis While Facilitating Proliferation, Migration, and Invasion Though Negative Regulation of the Camp/PKA Signaling Pathway via GLP1R

Qian¹,

Zhou²,

Chen³

et al. 2018

Cell Physiol Biochem

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“…Because the eight RNAs were not efficiently solubilized by a standard extraction method using phenol and guanidinium thiocyanate ( Fig 3A and B), like NEAT1, they are likely to form strong and extensive RNA-protein and protein-protein interactions in the cell. Among these RNAs, LINC00473, PVT1, and CCAT1 have been reported to play roles in specific tissue development and cancer progression, although their specific molecular functions remain poorly characterized (Tseng et al, 2014;Chen et al, 2016;Liang et al, 2016;McCleland et al, 2016). NEAT1, which is also involved in cancer progression and tissue development (Chakravarty et al, 2014;Nakagawa et al, 2014;Standaert et al, 2014;Adriaens et al, 2016), sequesters various RNAbinding proteins, transcription factors, and specific RNAs (Prasanth et al, 2005;Chen & Carmichael, 2009;Hirose et al, 2014b;Imamura et al, 2014;West et al, 2016) and/or associates with specific active chromosomal loci (West et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Unusual semi‐extractability as a hallmark of nuclear body‐associated architectural noncoding RNAs

et al. 2017

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long noncoding RNA (lncRNA) is the molecular scaffold of paraspeckle nuclear bodies. Here, we report an improved RNA extraction method: extensive needle shearing or heating of cell lysate in RNA extraction reagent improved extraction by 20-fold (a property we term "semi-extractability"), whereas using a conventional method was trapped in the protein phase. The improved extraction method enabled us to estimate that approximately 50 molecules are present in a single paraspeckle. Another architectural lncRNA,, also exhibited similar semi-extractability. A comparison of RNA-seq data from needle-sheared and control samples revealed the existence of multiple semi-extractable RNAs, many of which were localized in subnuclear granule-like structures. The semi-extractability of correlated with its association with paraspeckle proteins and required the prion-like domain of the RNA-binding protein FUS This observation suggests that tenacious RNA-protein and protein-protein interactions, which drive nuclear body formation, are responsible for semi-extractability. Our findings provide a foundation for the discovery of the architectural RNAs that constitute nuclear bodies.

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“…In the case of LAD, several lncRNAs, such as SPRY4-IT1, LINC01133, AGAP2-AS1, and LINC00473, have been characterised and their function have been reported in NSCLC as well as underlying mechanisms [20–23]. We previously showed that lncRNA PVT1 is significantly upregulated in LAD tissues and cells, and that it promotes cell proliferation through epigenetically repressing tumor suppressor LATS2 expression by interacting with EZH2 [13].…”

Section: Discussionmentioning

confidence: 99%

Long intergenic non-coding RNA 00152 promotes lung adenocarcinoma proliferation via interacting with EZH2 and repressing IL24 expression

et al. 2017

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BackgroundNumerous studies have shown that long non-coding RNAs (lncRNAs) behave as a novel class of transcript during multiple cancer processes, such as cell proliferation, apoptosis, migration, and invasion. LINC00152 is located on chromosome 2p11.2, and has a transcript length of 828 nucleotides. The biological role of LINC00152 in LAD(lung adenocarcinoma) remains unknown.MethodsQuantitative reverse transcription PCR(qRT-PCR) was used to detect LINC00152 expression in 60 human LAD tissues and paired normal tissues. In vitro and in vivo studies showed the biological function of LINC00152 in tumour progression. RNA transcriptome sequencing technology was performed to identify the downstream suppressor IL24(interleukin 24) which was further examined by qRT-PCR, western bolt and rescue experiments. RNA immunoprecipitation (RIP), RNA pulldown, and Chromatin immunoprecipitation (ChIP) assays were carried out to reveal the interaction between LINC00152, EZH2 and IL24.ResultsLINC00152 expression was upregulated in 60 human LAD tissues and paired normal tissues. High levels of LINC00152 expression were correlated with advanced TNM stage, larger tumor size, and lymph node metastasis, as well as shorter survival time. Silencing of LINC00152 suppressed cell growth and induced cell apoptosis. LINC00152 knockdown altered the expression of many downstream genes, including IL24. LINC00152 could interact with EZH2 and inhibit IL24 transcription. Moreover, the ectopic expression of IL24 repressed cell proliferation and partly reversed LINC00152 overexpression-induced promotion of cell growth in LAD.ConclusionsOur study reveals an oncogenic role for LINC00152 in LAD tumorigenesis, suggesting that it could be used as a therapeutic target in LAD treatment.Electronic supplementary materialThe online version of this article (doi:10.1186/s12943-017-0581-3) contains supplementary material, which is available to authorized users.

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Non-coding RNA LINC00473 mediates decidualization of human endometrial stromal cells in response to cAMP signaling

Cited by 51 publications

References 32 publications

LINC01121 Inhibits Cell Apoptosis While Facilitating Proliferation, Migration, and Invasion Though Negative Regulation of the Camp/PKA Signaling Pathway via GLP1R

LINC01121 Inhibits Cell Apoptosis While Facilitating Proliferation, Migration, and Invasion Though Negative Regulation of the Camp/PKA Signaling Pathway via GLP1R

Unusual semi‐extractability as a hallmark of nuclear body‐associated architectural noncoding RNAs

Long intergenic non-coding RNA 00152 promotes lung adenocarcinoma proliferation via interacting with EZH2 and repressing IL24 expression

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