Lnc<scp>RNA</scp> B4<scp>GALT</scp>1‐<scp>AS</scp>1 recruits HuR to promote osteosarcoma cells stemness and migration <i>via</i> enhancing <scp>YAP</scp> transcriptional activity

Li, Zhikun; Wang, Yi; Hu, Ruixi; Xu, Ruijun; Xu, Wei

doi:10.1111/cpr.12504

Cited by 57 publications

(74 citation statements)

References 33 publications

(38 reference statements)

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“…been shown to regulate YAP activity [19,20,26], it is assumed that MALAT1 could regulate YAP transcriptional activity. As the transcriptional factor YAP plays a critical role in the expansion of CSCs and lncRNA has 2 GyÁmin À1 radiation followed by detecting the cell viability.…”

Section: Malat1 Directly Binds To Yap Enhances Yap Protein Expressiomentioning

confidence: 99%

Retracted: Long noncoding RNA MALAT1 promotes the stemness of esophageal squamous cell carcinoma by enhancing YAP transcriptional activity

Yang

Liu

et al. 2019

FEBS Open Bio

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The tumor promoting roles of long noncoding RNA (lncRNA) MALAT1 have been revealed in various cancers; however, its roles in esophageal squamous cell carcinoma (ESCC) have not previously been disclosed. In this study, we found that MALAT1 expression was remarkably increased in ESCC cells compared to normal human esophageal epithelial cells. In addition, knockdown of MALAT1 attenuated the stemness of ESCC cells, as evidenced by a decrease in spheroid formation capacity, stemness marker expression and aldehyde dehydrogenase 1 activity. Moreover, MALAT1 knockdown decreased the migration ability of ESCC cells. Notably, knockdown of MALAT1 enhanced the radiosensitivity and chemosensitivity of ESCC cells. We also established that MALAT1 binds directly to Yes‐associated protein (YAP), thereby enhancing YAP protein expression and increasing YAP transcriptional activity. Overexpression of YAP partially rescued the effect of MALAT1 knockdown on stemness and radiosensitivity of ESCC cells. Overall, this study has identified that a novel MALAT1–YAP axis promotes the stemness of ESCC cells, and thus could be a potential target for treatment of ESCC.

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Section: Malat1 Directly Binds To Yap Enhances Yap Protein Expressiomentioning

confidence: 99%

Retracted: Long noncoding RNA MALAT1 promotes the stemness of esophageal squamous cell carcinoma by enhancing YAP transcriptional activity

Yang

Liu

et al. 2019

FEBS Open Bio

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“…LncRNAs could function by different pathways, such as lncRNAs serve as the protein co‐activators or co‐repressors, and thus the co‐regulators of mRNA and DNA . Recent studies have revealed the ceRNA roles of lncRNAs .…”

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA ANRIL enhances mitochondrial function of hepatocellular carcinoma by regulating the MiR‐199a‐5p/ARL2 axis

Bao

Wei

et al. 2019

Environmental Toxicology

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Although the roles of long non-coding RNA (lncRNA) ANRIL (Antisense non-coding RNA in the INK4A locus) have been established in various tumors, its roles in mitochondrial metabolic reprogramming of hepatocellular carcinoma (HCC) cells are still unclear. This work aims to explore lncRNA ANRIL roles in regulating the mitochondrial metabolic reprogramming of liver cancer cells. First, we found that lncRAN ANRIL expression was significantly increased in HCC tissues or cells compared with the normal adjacent tissues and normal tissues or cells. Functional experiment showed that overexpression of lncRNA ANRIL promoted mitochondrial function in HCC cells, evident by the increased mitochondrial DNA copy numbers, ATP (Adenosine triphosphate) level, mitochondrial membrane potential, and the expression levels of mitochondrial markers, while ANRIL knockdown exerted the opposite effects. Mechanistically, lncRNA ANRIL acted as a competing endogenous RNA to increase ARL2 (ADP-ribosylationfactor-like 2) expression via sponging miR-199a-5p. Notably, the miR-199a-5p/ARL2 axis is necessary for ANRIL-mediated promoting effects on HCC cell mitochondrial function. This work reveals a novel ANRIL-miR-199a-5p-ARL2 axis in HCC cell progression, which might provide potential targets for HCC treatment. K E Y W O R D SANRIL, ARL2, ceRNA, hepatocellular carcinoma, lncRNA, miR-199a-5p

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“…Originally, it was shown that a few lncRNAs are abnormally expressed in osteosarcoma (Li et al, 2013;Li et al, 2016). Subsequently, a large number of lncRNAs have been demonstrated to play an important role in the activities of osteosarcoma (Li et al, 2018;Huang et al, 2018;Deng et al, 2019). Furthermore, some lncRNAs have been demonstrated to be associated with the chemoresistance and overall survival of patients (Zhu et al, 2015;Chen et al, 2018;Chen et al, 2018).…”

Section: Discussionmentioning

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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LncRNA B4GALT1‐AS1 recruits HuR to promote osteosarcoma cells stemness and migration via enhancing YAP transcriptional activity

Abstract: We indicate that lncRNA B4GALT1-AS1 promotes OS cells stemness and migration via recruiting HuR to enhance YAP activity.

Cited by 57 publications

References 33 publications

Retracted: Long noncoding RNA MALAT1 promotes the stemness of esophageal squamous cell carcinoma by enhancing YAP transcriptional activity

Retracted: Long noncoding RNA MALAT1 promotes the stemness of esophageal squamous cell carcinoma by enhancing YAP transcriptional activity

Long non‐coding RNA ANRIL enhances mitochondrial function of hepatocellular carcinoma by regulating the MiR‐199a‐5p/ARL2 axis

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

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