Upregulation of long noncoding RNA Xist promotes proliferation of osteosarcoma by epigenetic silencing of P21

Xu, Tianyang; Jiang, Weihang; Fan, Lin; Gao, Qiuming; Li, Guodong

doi:10.18632/oncotarget.20738

Cited by 26 publications

(18 citation statements)

References 24 publications

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“…Recent studies demonstrated that XIST was associated with tumorigenesis, apoptosis, metastasis, and chemo‐ and radioresistance of cancers. Among them, XIST has been implicated to be upregulated in osteosarcoma (Gao et al, 2019; Lv, Miao, & Zhang, 2018; Li et al, 2019; Xu, Jiang, Fan, Gao, & Li, 2017; C. Yang et al, 2018), leading to the promotion of cell growth, migration, and invasion by targeting multiple signaling molecules. Our study demonstrated an oncogenic role of XIST in OS tumors and cells.…”

Section: Discussionmentioning

confidence: 99%

LncRNA‐XIST promotes the oxidative stress‐induced migration, invasion, and epithelial‐to‐mesenchymal transition of osteosarcoma cancer cells through miR‐153‐SNAI1 axis

Wen

Jiang

et al. 2020

Cell Biology International

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Osteosarcoma (OS) is the most common type of primary bone tumor that exhibits invasive growth and long‐distance organ metastasis. Thus, investigating the specifically targeted therapeutic agents against metastatic osteosarcoma depends on understanding the molecular mechanisms. The long noncoding RNAs (lncRNA) XIST (X‐inactive specific transcript) has been reported to have oncogenic roles in various malignant tumors including OS. However, its molecular mechanisms in OS migration and invasion are still under investigation. In the current study, we demonstrate that XIST is significantly upregulated in 30 pairs of OS tissues compared with their matched adjacent nontumor tissues by the quantitative reverse transcription polymerase chain reaction. Overexpression of XIST significantly induced the invasion, migration, and the epithelial‐to‐mesenchymal transition (EMT) phenotype. The epithelial marker, E‐cadherin was effectively suppressed by XIST overexpression. On the other way, the mesenchymal marker, Fibronectin, Snail, and Vimentin were significantly activated by exogenous XIST overexpression. Furthermore, we observed XIST was upregulated by the oxidative stress‐induced EMT. Bioinformatical analysis indicated that miR‐153 has multiple biding sites for XIST and miR‐153 was inversely suppressed by oxidative stress. XIST was verified to directly downregulate miR‐153 via sponging. We identified the mesenchymal marker, SNAI1 was a direct messenger RNA target of miR‐153. Importantly, inhibiting XIST successfully blocked the H2O2‐induced EMT of OS cells. In conclusion, this work demonstrates that lncRNA‐XIST promotes the oxidative stress‐induced OS cell invasion, migration, and EMT through the miR‐153/SNAI1 pathway, presenting lncRNA‐XIST as a promising therapeutic target for treating metastatic OS.

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Section: Discussionmentioning

confidence: 99%

LncRNA‐XIST promotes the oxidative stress‐induced migration, invasion, and epithelial‐to‐mesenchymal transition of osteosarcoma cancer cells through miR‐153‐SNAI1 axis

Wen

Jiang

et al. 2020

Cell Biology International

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“…Recent studies have reported that some lncRNAs, including Xist, APTR, and ANCR, can recruit EZH2 to epigenetically silence the cdkn1a (cyclin-dependent kinase inhibitor 1A, p21) gene, thereby promoting cell proliferation (39)(40)(41). p21 is an important cell-cycle regulator that restrains the cell cycle by inhibiting CDKs in mouse embryonic fibroblasts (42,43).…”

Section: Syisl Ko In Mice Significantly Increases Muscle Fiber Densitmentioning

confidence: 99%

Long noncoding RNA SYISL regulates myogenesis by interacting with polycomb repressive complex 2

Jin

Pan

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

108

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Although many long noncoding RNAs (lncRNAs) have been identified in muscle, their physiological function and regulatory mechanisms remain largely unexplored. In this study, we systematically characterized the expression profiles of lncRNAs during C2C12 myoblast differentiation and identified an intronic lncRNA, SYISL (SYNPO2 intron sense-overlapping lncRNA), that is highly expressed in muscle. Functionally, SYISL promotes myoblast proliferation and fusion but inhibits myogenic differentiation. SYISL knockout in mice results in significantly increased muscle fiber density and muscle mass. Mechanistically, SYISL recruits the enhancer of zeste homolog 2 (EZH2) protein, the core component of polycomb repressive complex 2 (PRC2), to the promoters of the cell-cycle inhibitor gene p21 and muscle-specific genes such as myogenin (MyoG), muscle creatine kinase (MCK), and myosin heavy chain 4 (Myh4), leading to H3K27 trimethylation and epigenetic silencing of target genes. Taken together, our results reveal that SYISL is a repressor of muscle development and plays a vital role in PRC2-mediated myogenesis.

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“…Lately, the binding relationship between long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) and EZH2 in osteosarcoma has been proposed [14]. Identified as an oncogene, lncRNA XIST has been reported to be abnormally expressed in diverse cancers and related to tumor development and progression [15].…”

Section: Introductionmentioning

confidence: 99%

LncRNA XIST facilitates cell growth, migration and invasion via modulating H3 histone methylation of DKK1 in neuroblastoma

Zhang

Yang

et al. 2019

Cell Cycle

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Long non-coding RNAs (lncRNAs) have been confirmed to be aberrantly expressed and involved in the progression of neuroblastoma. This study aimed to explore the expression profile of lncRNA X-inactive specific transcript (XIST) and its functional involvement in neuroblastoma. In this study, the relative level of XIST in neuroblastoma tissues and cell lines was detected by qPCR, and DKK1 protein expression was determined using western blot. The effect of XIST on cell growth, invasion and migration in vitro and in tumorigenesis of neuroblastoma was assessed. The level of H3K27me3 in DKK1 promoter was analyzed with ChIP-qPCR. Interaction between XIST and EZH2 was verified by RNA immunoprecipitation (RIP) and RNA pull-down assay. XIST was significantly upregulated in neuroblastoma tissues (n = 30) and cells lines, and it was statistically associated with the age and International Neuroblastoma Staging System (INSS) staging in neuroblastoma patients. Downregulation of XIST suppressed the growth, migration and invasion of neuroblastoma cells. EZH2 inhibited DKK1 expression through inducing H3 histone methylation in its promoter. XIST increased the level of H3K27me3 in DKK1 promoter via interacting with EZH2. Downregulation of XIST increased DKK1 expression to suppress neuroblastoma cell growth, invasion, and migration, which markedly restrained the tumor progression. In conclusion, XIST downregulated DKK1 by inducing H3 histone methylation via EZH2, thereby facilitating the growth, migration and invasion of neuroblastoma cells and retarding tumor progression.

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Upregulation of long noncoding RNA Xist promotes proliferation of osteosarcoma by epigenetic silencing of P21

Cited by 26 publications

References 24 publications

LncRNA‐XIST promotes the oxidative stress‐induced migration, invasion, and epithelial‐to‐mesenchymal transition of osteosarcoma cancer cells through miR‐153‐SNAI1 axis

LncRNA‐XIST promotes the oxidative stress‐induced migration, invasion, and epithelial‐to‐mesenchymal transition of osteosarcoma cancer cells through miR‐153‐SNAI1 axis

Long noncoding RNA SYISL regulates myogenesis by interacting with polycomb repressive complex 2

LncRNA XIST facilitates cell growth, migration and invasion via modulating H3 histone methylation of DKK1 in neuroblastoma

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