RETRACTED ARTICLE: Linc00152 promotes malignant progression of glioma stem cells by regulating miR-103a-3p/FEZF1/CDC25A pathway

Yu, Mingjun; Xue, Yixue; Zheng, Jian; Liu, Xiaobai; Yu, Hai; Liu, Libo; Li, Zhen; Liu, Yunhui

doi:10.1186/s12943-017-0677-9

Cited by 114 publications

(120 citation statements)

References 63 publications

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“…We subsequently confirmed that LINC00152 knockdown significantly suppresses glioma cell proliferation, migration, invasion, and tumor growth. Our results on the oncogenic role of LINC00152 are similar to the findings in a recently published paper by Yu and colleagues, where LINC00152 facilitated cell proliferation, migration, and invasion, while suppressing apoptosis in glioma stem cells by regulating the miR-103a-3p–FEZF1–CDC25A pathway [22]. …”

Section: Discussionsupporting

confidence: 90%

Long Intergenic Noncoding RNA 00152 Promotes Glioma Cell Proliferation and Invasion by Interacting with MiR-16

Chen¹,

Li²,

Gao³

et al. 2018

Cell Physiol Biochem

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Background/Aims: Long noncoding RNAs (lncRNAs) are a novel class of protein-noncoding transcripts that are aberrantly expressed in multiple diseases including cancers. LINC00152 has been identified as an oncogene involved in many kinds of cancer; however, its expression pattern and function in human glioma remain unclear. Methods: Quantitative real-time polymerase chain reaction was carried out to measure LINC00152 expression in human glioma cell lines and tissues. CCK-8 and EdU assays were performed to assess cell proliferation, and scratch assays and Transwell assays were used to assess cell migration and invasion, respectively. Luciferase reporter assays were carried out to determine the interaction between miR-16 and LINC00152. In vivo experiments were conducted to assess tumor formation. Results: LINC00152 was found to be significantly upregulated in human glioma cell lines and clinical samples. Knockdown of LINC00152 suppressed glioma cell proliferation, migration, and invasion in vitro. In vivo assays in nude mice confirmed that LINC00152 knockdown inhibits tumor growth. Furthermore, mechanistic investigation showed that LINC00152 binds to miR-16 in a sequence-specific manner and suppresses its expression. miR-16 inhibition strongly attenuated LINC00152 knockdown–mediated suppressive effects on proliferation, migration, and invasion. Moreover, LINC00152 induced BMI1 expression by sponging miR-16; this effect further promoted glioma cell proliferation and invasion. Conclusion: We regard LINC00152 as an oncogenic lncRNA promoting glioma cell proliferation and invasion and as a potential target for human glioma treatment.

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Section: Discussionsupporting

confidence: 90%

Long Intergenic Noncoding RNA 00152 Promotes Glioma Cell Proliferation and Invasion by Interacting with MiR-16

Chen¹,

Li²,

Gao³

et al. 2018

Cell Physiol Biochem

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“…[29] Recent studies have shown that LINC00152 is highly expressed in a variety of tumors, such as, glioma, [30] nonsmall cell lung cancer, [31] gastric cancer, [32] etc. [29] Recent studies have shown that LINC00152 is highly expressed in a variety of tumors, such as, glioma, [30] nonsmall cell lung cancer, [31] gastric cancer, [32] etc.…”

Section: Discussionmentioning

confidence: 99%

Targeting YAP1/LINC00152/FSCN1 Signaling Axis Prevents the Progression of Colorectal Cancer

Sun

et al. 2019

Advanced Science

125

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cancer-associated lncRNA (CCAL), [3] colon cancer-associated transcript 1 (CCAT1) and colon cancer-associated transcript 2 (CCAT2). [4] Since lncRNAs regulate a subset of genes, and are transcriptionally regulated by a series of transcription factors, targeting these lncRNAs induces a much greater effect on cancer cells than targeting single gene. [5] Therefore, exploring the upstream and downstream regulation mechanism of cancer-associated lncRNAs has been gaining widespread attention.As the main effector of the Hippo pathway, Yes-associated protein 1 (YAP1) plays a key role in regulating multiple biological function, including cell-cell contact inhibition, proliferation, and differentiation. [6,7] As a transcription coactivator, YAP1 is abnormally expressed in various malignancies, [8,9] and modulates biological phenotypes of cancer cells via regulating a number of target genes, such as CTGF, CYR61, and AREG. [7,8] Recently, a novel regulatory model of YAP1 transcriptionally regulating the noncoding RNAs (ncRNAs) in CRC has attracted much attention, in which of these noncoding RNAs, including microRNAs (miR-130a [10] and miR-29 [11] ), as well as lncRNAs (RMRP, [12] BCAR4, [13] MALAT1, [14] and lncARSR [15] ). However, the mechanism and As a transcription coactivator, Yes-associated protein 1 (YAP1)'s role in tumorigenesis is well established. However, the mechanism of YAP1-regulating long noncoding RNAs (lncRNA) in tumors is still largely unknown. Here, a YAP1 target gene, long intergenic noncoding RNA 00152 (LINC00152), which is highly expressed in colorectal cancer (CRC), is identified. The oncogenic functions of LINC00152 in CRC are demonstrated by a panel of in vitro and in vivo experiments. Further studies reveal the potential downstream mechanisms of LINC00152, which can act as a competing endogenous RNA sponging with miR-632 and miR-185-3p to regulate Fascin actin-bundling protein 1 (FSCN1) expression and thus promote the malignant proliferation and metastasis in CRC cells. Targeting the YAP1/LINC00152/ FSCN1 axis inhibits the progression of CRC. This finding provides a new regulatory model of the "YAP1-lncRNA" in CRC, which gives rise to a new perspective, "YAP1/LINC00152/miR-632-miR-185-3p/FSCN1," to explore the cancer-promoting mechanism of YAP1 involved in CRC.

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“…Glioma cells were cultured in Dulbecco's modified Eagle medium (DMEM)/high glucose with 10% fetal bovine serum (FBS, Gibco, Carlsbad, CA, USA) and were maintained in a humidified incubator at 37°C with 5% CO 2 . GSCs were separated as described previously from tissue cells . Primary cells were detached with trypsin, washed once in FACs buffer (PBS containing 1%‐2% BSA and 5 mM EDTA), then stained with anti‐CD24‐FITC (Invitrogen, Carlsbad, CA, USA) and anti‐CD133‐PE (Invitrogen) using 10 μl of antibody per 10 6 cells, and incubated at 4°C for 15 minutes.…”

Section: Methodsmentioning

confidence: 99%

LncRNA MALAT1/miR‐129 axis promotes glioma tumorigenesis by targeting SOX2

Zhang

Wang

et al. 2018

J Cellular Molecular Medi

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We aimed to explore the interaction among lncRNA MALAT1, miR‐129 and SOX2. Besides, we would investigate the effect of MALAT1 on the proliferation of glioma stem cells and glioma tumorigenesis. Differentially expressed lncRNAs in glioma cells and glioma stem cells were screened out with microarray analysis. The targeting relationship between miR‐129 and MALAT1 or SOX2 was validated by dual‐luciferase reporter assay. The expressions of MALAT1, miR‐129 and SOX2 mRNA in both glioma non‐stem cells and glioma stem cells were examined by qRT‐PCR assay. The impact of MALAT1 and miR‐129 on glioma stem cell proliferation was observed by CCK‐8 assay, EdU assay and sphere formation assay. The protein expression of SOX2 was determined by western blot. The effects of MALAT1 and miR‐129 on glioma tumour growth were further confirmed using xenograft mouse model. The mRNA expression of MALAT1 was significantly up‐regulated in glioma stem cells compared with non‐stem cells, while miR‐129 was significantly down‐regulated in glioma stem cells. MALAT1 knockdown inhibited glioma stem cell proliferation via miR‐129 enhancement. Meanwhile, miR‐129 directly targeted at SOX2 and suppressed cell viability and proliferation of glioma stem cells by suppressing SOX2 expression. The down‐regulation of MALAT1 and miR‐129 overexpression both suppressed glioma tumour growth via SOX2 expression promotion in vivo. MALAT1 enhanced glioma stem cell viability and proliferation abilities and promoted glioma tumorigenesis through suppressing miR‐129 and facilitating SOX2 expressions.

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RETRACTED ARTICLE: Linc00152 promotes malignant progression of glioma stem cells by regulating miR-103a-3p/FEZF1/CDC25A pathway

Cited by 114 publications

References 63 publications

Long Intergenic Noncoding RNA 00152 Promotes Glioma Cell Proliferation and Invasion by Interacting with MiR-16

Long Intergenic Noncoding RNA 00152 Promotes Glioma Cell Proliferation and Invasion by Interacting with MiR-16

Targeting YAP1/LINC00152/FSCN1 Signaling Axis Prevents the Progression of Colorectal Cancer

LncRNA MALAT1/miR‐129 axis promotes glioma tumorigenesis by targeting SOX2

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