<scp>LINC</scp>00152: A pivotal oncogenic long non‐coding <scp>RNA</scp> in human cancers

Yu, Yang; Yang, Jian; Li, Quanpeng; Xu, Boming; Lian, Yifan; Ma, Lin

doi:10.1111/cpr.12349

Cited by 80 publications

(74 citation statements)

References 55 publications

(73 reference statements)

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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

122

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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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Section: Discussionmentioning

confidence: 99%

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

Sun

et al. 2019

Advanced Science

122

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“…LncRNAs have emerged as possible biological regulators of a wide range of cellular activities such as proliferation, apoptosis, migration, and invasion [19]. Over the past several years, emerging data showed that alterations in the expression of lncRNAs contribute to the pathogenesis of many human cancers, where they function as either oncogenes or tumor suppressors [20].…”

Section: Discussionmentioning

confidence: 99%

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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“…ncRNAs are essential for the regulation and execution of key cellular processes, including proliferation, apoptosis, autophagy, differentiation, metabolism, migration, differentiation and invasion . It therefore comes as no surprise that ncRNAs are deregulated in most, if not all, kinds of diseases, including neoplastic, inflammatory and metabolic diseases . From a clinical perspective, the frequent alteration of ncRNA abundance in the body fluid, such as saliva, blood and urine, during diseases make this class of molecules promising candidates for development into biomarkers for early diagnosis and prognostication …”

Section: Introductionmentioning

confidence: 99%

Emerging roles of non‐coding RNAs in scoliosis

Shen

et al. 2019

Cell Proliferation

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Scoliosis, a complex three‐dimensional deformity of the spine with the Cobb angle (a measure of the spinal lateral curvature) >10 degree, encompasses a spectrum of pathologies, including congenital, idiopathic, syndromic and neuromuscular aetiologies. The pathogenesis is multifactorial involving both environmental and genetic factors but the exact cellular and molecular mechanisms of disease development remain largely unknown. Emerging evidence showed that non‐coding RNAs (ncRNAs), namely microRNAs, long ncRNAs and circular RNAs, are deregulated in many orthopaedic diseases, including scoliosis. Importantly, these deregulated ncRNAs functionally participate in the initiation and progression of scoliosis. Here, we review recent progress in ncRNA research on scoliosis.

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LINC00152: A pivotal oncogenic long non‐coding RNA in human cancers

Cited by 80 publications

References 55 publications

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

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

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

Emerging roles of non‐coding RNAs in scoliosis

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