Increased expression of long noncoding RNA GAS6‐AS2 promotes proliferation and inhibits apoptosis of melanoma cells via upregulating GAS6 expression

Wen, Li; Zheng, Yuanquan; Wen, Xiaoyi; Zhang, Yitian; Zeng, Weihui

doi:10.1002/iub.2071

Cited by 15 publications

(12 citation statements)

References 40 publications

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“…Given that the levels of GAS6-AS2 in OS were distinctly up-regulated, we supposed GAS6-AS2 as a contributor in this tumor. Previous study by Wen et al showed that knockdown of GAS6-AS2 suppressed the proliferation and metastasis of melanoma cells, suggesting that GAS6-AS2 as a tumor promoter in this disease [16]. In this study, we also down-regulated the expressions of GAS6-AS2 in MG63 and 143B for the study of GAS6-AS2 function.…”

Section: Discussionmentioning

confidence: 50%

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USF1-mediated upregulation of lncRNA GAS6-AS2 facilitates osteosarcoma progression through miR-934/BCAT1 axis

Wei

Zhang

et al. 2020

Aging

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Long noncoding RNAs (lncRNAs) have been certified as important regulators in tumorigenesis. LncRNA GAS6-AS2 (GAS6-AS2) was a newly identified tumor-related lncRNA, and its dysregulation and oncogenic effects in melanoma and bladder cancer had been reported in previous studies. However, the expression pattern and potential function of GAS6-AS2 in osteosarcoma (OS) have not been investigated. In this study, we identified a novel OS-related lncRNA GAS6-AS2. We found that GAS6-AS2 was distinctly upregulated in both OS specimens and cell lines. Distinct up-regulation of GAS6-AS2 in OS was correlated with advanced clinical stages and shorter survivals. In addition, USF1 could directly bind to the GAS6-AS2 promoter and contribute to its overexpression. Furthermore, GAS6-AS2 knockdown caused tumor suppressive effects via reducing cellular proliferation, migration and invasion, and promoting OS cell apoptosis. Besides, GAS6-AS2 directly bound to miR-934 and downregulated its expression. Mechanistically, GAS6-AS2 positively regulated the expression of BCAT1 through sponging miR-934. Taken together, our data illustrated how GAS6-AS2 played an oncogenic role in OS and might offer a potential therapeutic target for treating OS.

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Section: Discussionmentioning

confidence: 50%

“…Previous studies have confirmed that GAS6-AS2 was highly expressed in melanoma and bladder cancer tissues [15,16]. However, the potential mechanism involved in the upregulation of GAS6-AS2 in the above tumors has not been investigated.…”

Section: Discussionmentioning

confidence: 94%

USF1-mediated upregulation of lncRNA GAS6-AS2 facilitates osteosarcoma progression through miR-934/BCAT1 axis

Wei

Zhang

et al. 2020

Aging

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“…Furthermore, the alteration of LINC00261, C4A, and C4B following valproic acid treatment in motor neurons ( Yoshida et al, 2015 ), as well as the clustering of AC025280.2 with neuron-related genes ( Tenjin et al, 2020 ), suggest the possible role of these genes in neuron development. Additionally, while the expression and function of GAS6-DT in neurons and the brain remain unclear, there is evidence that GAS6-DT is involved in the upregulation of GAS6 gene expression in melanomas ( Wen et al, 2019 ). GAS6 is also a protein-coding hub gene associated with maturation (kME > 0.90), with roles in the central nervous system (CNS) ( Goudarzi et al, 2016 ), and highlighting a similar crosstalk between GAS6 and GAS6-DT can influence neuron development and maturation in the context of iPSC-derived neuron generation.…”

Section: Resultsmentioning

confidence: 99%

Transcriptome Dynamics of Human Neuronal Differentiation From iPSC

Kuruş

Akbari

Eskier

et al. 2021

Front. Cell Dev. Biol.

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The generation and use of induced pluripotent stem cells (iPSCs) in order to obtain all differentiated adult cell morphologies without requiring embryonic stem cells is one of the most important discoveries in molecular biology. Among the uses of iPSCs is the generation of neuron cells and organoids to study the biological cues underlying neuronal and brain development, in addition to neurological diseases. These iPSC-derived neuronal differentiation models allow us to examine the gene regulatory factors involved in such processes. Among these regulatory factors are long non-coding RNAs (lncRNAs), genes that are transcribed from the genome and have key biological functions in establishing phenotypes, but are frequently not included in studies focusing on protein coding genes. Here, we provide a comprehensive analysis and overview of the coding and non-coding transcriptome during multiple stages of the iPSC-derived neuronal differentiation process using RNA-seq. We identify previously unannotated lncRNAs via genome-guided de novo transcriptome assembly, and the distinct characteristics of the transcriptome during each stage, including differentially expressed and stage specific genes. We further identify key genes of the human neuronal differentiation network, representing novel candidates likely to have critical roles in neurogenesis using coexpression network analysis. Our findings provide a valuable resource for future studies on neuronal differentiation.

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“…A number of lncRNAs have been shown to be differentially expressed in melanoma [29][30][31]. Several studies have also validated the relationship between dysregulated lncRNAs and melanoma pathogenesis, with these regulatory actions being mediated by multiple mechanistic interactions [32][33][34].…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA LINC01291 promotes the aggressive properties of melanoma by functioning as a competing endogenous RNA for microRNA-625-5p and subsequently increasing IGF-1R expression

Lin

et al. 2021

Cancer Gene Ther

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Studies have confirmed the relationship between dysregulated long noncoding RNAs and melanoma pathogenesis. However, the regulatory functions of long intergenic non-protein coding RNA 1291 (LINC01291) in melanoma remain unknown. Therefore, we evaluated LINC01291 expression in melanoma and explored its roles in regulating tumor behaviors. Further, the molecular events via which LINC01291 affects melanoma cells were investigated. LINC01291 expression in melanoma cells was analyzed using The Cancer Genome Atlas database and quantitative real-time polymerase chain reaction. Functional assays, including the Cell Counting Kit-8 assay, colony formation assay, flow cytometry, cell migration and invasion assays, and tumor xenograft models, were used to examine LINC01291’s role in melanoma cells. Additionally, bioinformatics analysis, RNA immunoprecipitation, luciferase reporter assay, and western blotting were conducted to determine the tumor-promoting mechanism of LINC01291. LINC01291 was upregulated in melanoma tissues and cell lines. Following LINC01291 knockdown, cell proliferation, colony formation, migration, and invasion were diminished, whereas apoptosis was enhanced and the cell cycle was arrested at G0/G1. In addition, loss of LINC01291 decreased the chemoresistance of melanoma cells to cisplatin. Furthermore, LINC01291 interference inhibited melanoma tumor growth in vivo. Mechanistically, LINC01291 functions as a competing endogenous RNA by sponging microRNA-625-5p (miR-625-5p) in melanoma cells and maintaining insulin-like growth factor 1 receptor (IGF-1R) expression. Rescue experiments revealed that the roles induced by LINC01291 depletion in melanoma cells could be reversed by suppressing miR-625-5p or overexpressing IGF-1R. Our study identified the LINC01291/miR-625-5p/IGF-1R competing endogenous RNA pathway in melanoma cells, which may represent a novel diagnostic biomarker and an effective therapeutic target for melanoma.

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Increased expression of long noncoding RNA GAS6‐AS2 promotes proliferation and inhibits apoptosis of melanoma cells via upregulating GAS6 expression

Cited by 15 publications

References 40 publications

USF1-mediated upregulation of lncRNA GAS6-AS2 facilitates osteosarcoma progression through miR-934/BCAT1 axis

USF1-mediated upregulation of lncRNA GAS6-AS2 facilitates osteosarcoma progression through miR-934/BCAT1 axis

Transcriptome Dynamics of Human Neuronal Differentiation From iPSC

Long noncoding RNA LINC01291 promotes the aggressive properties of melanoma by functioning as a competing endogenous RNA for microRNA-625-5p and subsequently increasing IGF-1R expression

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