Long noncoding RNA LINC00152 is a potential prognostic biomarker in patients with high‐grade glioma

Wang, Wen; Wu, Fan; Zhao, Zheng; Wang, Kuanyu; Huang, Ruoyu; Wang, Hao‐Yuan; Lan, Qing; Wang, Jiangfei; Zhao, Jizong

doi:10.1111/cns.12850

Cited by 22 publications

(20 citation statements)

References 29 publications

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“…Interestingly, LINC00152 expression in doxorubicin-resistant MCF-7 breast cancer cells was significantly higher than that in the parental cells (Hu et al, 2018). Decreasing LINC00152 expression promoted chemosensitivity to temozolomide and enhanced survival of patients with high-grade glioma (Wang W et al, 2018). These results indicate that LINC00152 can serve as a predictor of chemoresistance.…”

Section: Effect Of Linc00152 On the Radiosensitivity Of Nsclc Cellsmentioning

confidence: 76%

Role of LINC00152 in non-small cell lung cancer

2020

J. Zhejiang Univ. Sci. B

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Non-small cell lung cancer (NSCLC) accounts for about 85% of all lung cancer cases. The pathogenesis of NSCLC involves complex gene networks that include different types of non-coding RNAs, such as long non-coding RNAs (lncRNAs). The role of lncRNAs in NSCLC is gaining an increasing interest as their function is being explored in various human cancers. Recently, a new oncogenic lncRNA, LINC00152 (cytoskeleton regulator RNA (CYTOR)), has been identified in different tumor types. In NSCLC, the high expression of LINC00152 in tumor tissue and peripheral blood samples has been shown to be associated with worse prognoses of NSCLC patients. Overexpression of LINC00152 has been confirmed to promote the proliferation, invasion, and migration of NSCLC cells in vitro, as well as increase tumor growth in vivo. This review discusses the role of LINC00152 in NSCLC.

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Section: Effect Of Linc00152 On the Radiosensitivity Of Nsclc Cellsmentioning

confidence: 76%

Role of LINC00152 in non-small cell lung cancer

2020

J. Zhejiang Univ. Sci. B

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“…The results show that, after over-expression of LINC00152, for U251 and U87 cells, their cell viability, colony formation ability and growing ability of subcutaneously transplanted tumors in mice are signi cantly enhanced, which is similar with the report of literature. [6] Further Immuno uorescence experiment shows that, under normal conditions, there are obvious YAP expression in cytoplasm and nuclei at U251 and U87 cells; however, after over-expression of LINC00152, the YAP expression of cytoplasm isn't obvious at two cells. It suggests that, LINC00152 can mediate cytoplasm YAP nuclear translocation at U251 and U87 cells.…”

Section: Discussionmentioning

confidence: 95%

“…It inhibits the growth of glioma cells in the subcutaneously transplanted tumors in the nude mice by down-regulating LINC00152 expression. [6] It suggests that, LINC00152 might have cancer promotion effect on glioma, and it promotes the in vivo growth of glioma cells.…”

Section: Discussionmentioning

confidence: 99%

“…[3][4][5] The latest clinical studies have shown that, LINC00152 is associated with poor clinical prognosis of brain glioma, and in the models of nude mouse with subcutaneously transplanted tumor, it is found that it helps inhibit the in vivo growth of brain glioma by down-regulating LINC00152 expression. [6] It suggests that, LINC00152 is associated with malignant biological behaviors of glioma cells, and it has cancer promoting effects. However, the cancer promoting mechanism of LINC00152 remain unclear, which requires further exploration.…”

Section: Introductionmentioning

confidence: 99%

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Long noncoding RNA LINC00152 promotes glioma cell proliferation via Src-YAP signaling pathway

Liang¹,

Lan²,

Jin³

et al. 2020

Preprint

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Objective The study is designed to observe the influence of LncRNA LINC00152 on the proliferation of glioma cells and explore the role of Src-YAP signal pathway in the process.Methods U251 and U87 cell were used for in vitro experiments and xenograft studies; transfection method was adopted to build a LINC00152 overexpressing cell strain, and cell viability was determined by MTT assay; cell colony formation ability was measured through colony formation assay, and protein expression was determined by Western blot; YAP protein expression distribution is detected through Immunofluorescence.Key findings LINC00152 overexpressing can enhance the U251 and U87 cell proliferation, the colony formation and the growing ability of subcutaneously transplanted tumor, and it induces YAP nuclear import and down-regulates p-LATS1 and p-YAP protein expression, and up-regulates p-Src protein expression. Src inhibitor 1 can inhibit the changes in protein expression and the cell colony formation of p-LATS1, p-YAP and p-Src, which are induced by overexpression of LINC00152 in U251 and U87 cells.Conclusions LINC00152 promotes cell proliferation of glioma U251 and U87, and the action might be associated with process of activation of Src, inhibition of phosphorylation cascade reaction of LATS1-YAP pathway and final inducing of YAP nuclear import.

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“…Moreover, lncRNAs regulate cellular growth, survival, and differentiation, genomic imprinting, epigenetic and post-transcriptional regulation of gene expression, alternate splicing, chromatin modifications, subcellular transport, and inflammatory mechanisms [ 11 – 14 ]. Dysregulation of lncRNAs is associated with the growth and metastasis of several tumors including gliomas [ 15 – 17 ]. The role of lncRNA FAM181A-AS1 in gliomas is not known.…”

Section: Introductionmentioning

confidence: 99%

LncRNA FAM181A-AS1 promotes gliomagenesis by sponging miR-129-5p and upregulating ZRANB2

Jiang

Chen

2020

aging

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In this study, we investigated the functional and clinical significance of the long non-coding RNA (lncRNA) FAM181A-AS1 in human gliomas. TCGA, GTEx and CGGA database analyses showed that high FAM181A-AS1 expression correlates with advanced tumor stage and poor survival of glioma patients. FAM181A-AS1 expression is higher in glioma cell lines compared to normal human astrocytes (NHA). CCK-8, EdU, and colony formation assays show that FAM181A-AS1 knockdown decreases proliferation and colony formation in glioma cells, whereas, FAM181A-AS1 overexpression reverses these effects. Bioinformatics analysis showed that miR-129-5p is a potential target of FAM181A-AS1. MiR-129-5p expression negatively correlates with FAM181A-AS1 expression in glioma patients. Dual luciferase reporter assays confirmed that miR-129-5p binds directly to FAM181A-AS1 in glioma cells. RNA immunoprecipitation (RIP) assays using anti-Ago2 antibody pulled down FAM181A-AS1 with miR-129-5p. Bioinformatics analysis identified ZRANB2 as a potential miR-129-5p target gene. Dual luciferase reporter assays confirmed that miR-129-5p binds directly to the 3’-UTR of ZRANB 2 mRNA. Furthermore, miR-129-5p overexpression or ZRANB2 knockdown reduces proliferation and colony formation of FAM181A-AS1 overexpressing glioma cells. These findings show that FAM181A-AS1 promotes gliomagenesis by enhancing ZRANB2 expression by sponging of miR-129-5p.

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Long noncoding RNA LINC00152 is a potential prognostic biomarker in patients with high‐grade glioma

Abstract: Our results indicate that knockdown of LINC00152 could inhibit tumor growth in vivo. LINC00152 could serve as a potential prognostic biomarker in patients with HGG.

Cited by 22 publications

References 29 publications

Role of LINC00152 in non-small cell lung cancer

Role of LINC00152 in non-small cell lung cancer

Long noncoding RNA LINC00152 promotes glioma cell proliferation via Src-YAP signaling pathway

LncRNA FAM181A-AS1 promotes gliomagenesis by sponging miR-129-5p and upregulating ZRANB2

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