<i>Retracted</i>: Long noncoding RNA Alu‐mediated p21 transcriptional regulator promotes proliferation, migration, and pipe‐formation of human microvascular endothelial cells by sponging miR‐126

Song, Ai-Ping; Feng, Ru; Gao, Jianying; Yang, Chunqing

doi:10.1002/jcb.29291

Cited by 4 publications

(3 citation statements)

References 31 publications

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“…Experimental studies have also found that lncRNAs can regulate EC gene expression; for instance, lncRNA-CCL2 upregulates the levels of its adjacent CCL2 gene, which is a pro-atherosclerotic chemokine gene in the EC lines. Further, the lncRNA APTR can promote the proliferation and migration of ECs ( 67 ). HULC can promote the apoptosis of ECs ( 35 ).…”

Section: Lncrna and Rbp As Regulators Of Atherosclerosismentioning

confidence: 99%

The Combined Regulation of Long Non-coding RNA and RNA-Binding Proteins in Atherosclerosis

Ding

Yin

Zhang

et al. 2021

Front. Cardiovasc. Med.

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Atherosclerosis is a complex disease closely related to the function of endothelial cells (ECs), monocytes/macrophages, and vascular smooth muscle cells (VSMCs). Despite a good understanding of the pathogenesis of atherosclerosis, the underlying molecular mechanisms are still only poorly understood. Therefore, atherosclerosis continues to be an important clinical issue worthy of further research. Recent evidence has shown that long non-coding RNAs (lncRNAs) and RNA-binding proteins (RBPs) can serve as important regulators of cellular function in atherosclerosis. Besides, several studies have shown that lncRNAs are partly dependent on the specific interaction with RBPs to exert their function. This review summarizes the important contributions of lncRNAs and RBPs in atherosclerosis and provides novel and comprehensible interaction models of lncRNAs and RBPs.

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Section: Lncrna and Rbp As Regulators Of Atherosclerosismentioning

confidence: 99%

The Combined Regulation of Long Non-coding RNA and RNA-Binding Proteins in Atherosclerosis

Ding

Yin

Zhang

et al. 2021

Front. Cardiovasc. Med.

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“…For example, APTR can recruit PRC2 to the p21 promoter of malignant glioma cells to inhibit p21 expression and accelerate tumor progression. 11 Silencing APTR in osteosarcoma cells inhibits cell proliferation, invasion, and migration. 12 APTR promotes the proliferation of leiomyoma cells by targeting the Era Wnt pathway.…”

Section: Introductionmentioning

confidence: 99%

The transcript NR 134251.1 of lncRNA APTR with an opposite function to all transcripts inhibits proliferation and induces apoptosis by regulating proliferation and apoptosis-related genes

Shen

et al. 2023

Hum Exp Toxicol

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Arsenic (As) exposure has been a global public health concern for hundreds of millions worldwide. LncRNA APTR (Alu-mediated p21 transcriptional regulator) plays an essential role in tumor growth and development. However, its function in arsenic-induced toxicological responses is still unknown. In this study, we found that the expressions of all transcripts and the transcript NR 134251.1 of APTR were increased in a dose-dependent manner in 16HBE cells treated with sodium arsenite (NaAsO2). Silencing the transcript NR 134251.1 of APTR inhibited cell proliferation and induced apoptosis. However, silencing all transcripts of APTR had the opposite function to the transcript NR 134251.1. Then we examined the protein level of the proliferation and apoptosis-related genes after silencing the transcript NR 134251.1 of APTR. The results showed that silencing the transcript NR 134251.1 of APTR up-regulated the expression of transcription factor E2F1 and regulated its downstream genes involved in proliferation and apoptosis, including p53, phospho-p53-S392, phospho-p53-T55, p21, Cyclin D1, PUMA, Fas, Bim, BIK, Caspase-3, Caspase-7, and Cyt-c. In conclusion, arsenic induced APTR expression and the transcript NR 134251.1 of APTR have an opposite function to all transcripts, providing a theoretical basis for the prevention and treatment of arsenic exposure.

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“…Long non-coding RNAs (lncRNAs) (> 200 nucleotides) are a class of RNA transcripts that can regulate gene expression but cannot code protein (Bu et al, 2012;Kung et al, 2013). LncRNAs have been reported to play a role in a variety of biological pathways (Jiapaer et al, 2018;Song et al, 2019) and disease states (Kung et al, 2013), including tumors (Gutschner and Diederichs, 2012). Recently, the role of lncRNAs in osteosarcoma pathogenesis has attracted much attention and is being heavily investigated, particularly through high-throughput sequencing.…”

Section: Introductionmentioning

confidence: 99%

LncRNA LINC00588 Suppresses the Progression of Osteosarcoma by Acting as a ceRNA for miRNA-1972

et al. 2020

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Long non-coding RNAs (lncRNAs) are being found to play an increasingly important role in the development of tumors. However, their biological functions and the underlying mechanisms remain unclear. Using information from GEO Datasets, we found that the lncRNA LINC00588 was downregulated in osteosarcoma (OS) in bone but was upregulated in the metastatic tumor present in the lung. We assessed the function of LINC00588 using both overexpression and knockout studies. We performed colony formation assay, CCK-8 assay, flow cytometry, wound healing assay, transwell assay, and RT-qPCR assay and used a xenograft model to investigate the influence of LINC00588 on cell proliferation, viability, cell apoptosis and cycle, migration, invasion, endothelial cell function, EMT (epithelial to mesenchymal transition), and tumor growth, respectively. Overexpression of LINC00588 appeared to inhibit cell proliferation, viability, migration, invasion, endothelial cell function, EMT, and tumor growth but not apoptosis, while we got the opposite result when we knocked down LINC00588. Next, we predicted that LINC00588 bound to miRNA-1972 and significantly downregulated its expression, which we then verified through a luciferase reporter assay. Subsequently, we knocked down miR1972 and performed CCK-8 and transwell assays to demonstrate that downregulation of miRNA-1972 could substantially inhibit the viability and invasion of osteosarcoma cells. The expression of TP53 was downregulated at the protein level but not at the mRNA level after the overexpression of miRNA-1972. Taken together, our findings indicate that LINC00588 plays a role in OS development by downregulating the expression of miRNA-1972, which can, in turn, inhibit the expression of TP53. Hence, we believe that the LINC00588/miRNA-1072/TP53 axis could potentially serve as a therapeutic target or diagnostic biomarker for osteosarcoma.

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Retracted: Long noncoding RNA Alu‐mediated p21 transcriptional regulator promotes proliferation, migration, and pipe‐formation of human microvascular endothelial cells by sponging miR‐126

Cited by 4 publications

References 31 publications

The Combined Regulation of Long Non-coding RNA and RNA-Binding Proteins in Atherosclerosis

The Combined Regulation of Long Non-coding RNA and RNA-Binding Proteins in Atherosclerosis

The transcript NR 134251.1 of lncRNA APTR with an opposite function to all transcripts inhibits proliferation and induces apoptosis by regulating proliferation and apoptosis-related genes

LncRNA LINC00588 Suppresses the Progression of Osteosarcoma by Acting as a ceRNA for miRNA-1972

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