LINC00152

In a study, Nötzold et al., performed a high-throughput siRNA screen targeting 638 lncRNAs deregulated in cancer entities to analyse their impact on cell division by using time-lapse microscopy. We identified 26 lncRNAs affecting cell morphology and cell cycle including LINC00152. This transcript was ubiquitously expressed in many human cell lines and its RNA levels were significantly upregulated in lung, liver and breast cancer tissues. A comprehensive sequence analysis of LINC00152 revealed a highly similar paralog annotated as MIR4435-2HG and several splice variants of both transcripts. The shortest and most abundant isoform preferentially localized to the cytoplasm. Cells depleted of LINC00152 arrested in prometaphase of mitosis and showed reduced cell viability. In RNA affinity purification (RAP) studies, LINC00152 interacted with a network of proteins that were associated with M phase of the cell cycle ¹⁾.

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.

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.

They regard LINC00152 as an oncogenic lncRNA promoting glioma cell proliferation and invasion and as a potential target for human glioma treatment ²⁾.

Retracted article

LINC00152 has been identified as an oncogene involved in many kinds of cancer; however, its expression pattern and function in human glioma remain unclear.

Linc00152/miR-103a-3p/FEZF1/CDC25A axis plays a novel role in regulating the malignant behavior of glioma stem cells (GSCs), which may be a new potential therapeutic strategy for glioma therapy ³⁾ ⁴⁾.

¹⁾

Nötzold L, Frank L, Gandhi M, Polycarpou-Schwarz M, Groß M, Gunkel M, Beil N, Erfle H, Harder N, Rohr K, Trendel J, Krijgsveld J, Longerich T, Schirmacher P, Boutros M, Erhardt S, Diederichs S. The long non-coding RNA LINC00152 is essential for cell cycle progression through mitosis in HeLa cells. Sci Rep. 2017 May 23;7(1):2265. doi: 10.1038/s41598-017-02357-0. PubMed PMID: 28536419; PubMed Central PMCID: PMC5442156.

²⁾

Chen X, Li D, Gao Y, Tang W, Iw L, Cao Y, Hao B. Long Intergenic Noncoding RNA 00152 Promotes Glioma Cell Proliferation and Invasion by Interacting with MiR-16. Cell Physiol Biochem. 2018 Apr 13;46(3):1055-1064. doi: 10.1159/000488836. [Epub ahead of print] PubMed PMID: 29669323.

³⁾

Yu M, Xue Y, Zheng J, Liu X, Yu H, Liu L, Li Z, Liu Y. Linc00152 promotes malignant progression of glioma stem cells by regulating miR-103a-3p/FEZF1/CDC25A pathway. Mol Cancer. 2017 Jun 26;16(1):110. doi: 10.1186/s12943-017-0677-9. PubMed PMID: 28651608; PubMed Central PMCID: PMC5485714.

⁴⁾

Yu M, Xue Y, Zheng J, Liu X, Yu H, Liu L, Li Z, Liu Y. Retraction Note to: Linc00152 promotes malignant progression of glioma stem cells by regulating miR-103a-3p/FEZF1/CDC25A pathway. Mol Cancer. 2022 Sep 29;21(1):188. doi: 10.1186/s12943-022-01660-3. PMID: 36175912.