LncRNA THOR promotes tongue squamous cell carcinomas by stabilizing IGF2BP1 downstream targets

Yang, Haojie; Fu, Ganglan; Liu, Funing; Hu, Chuwen; Lin, Junjie; Tan, Zicong; Fu, Yanni; Ji, Fengtao; Cao, Minghui

doi:10.1016/j.biochi.2019.06.012

Cited by 27 publications

(15 citation statements)

References 34 publications

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“…Regarding TScc, recent studies have indicated that numerous lncRNAs are abnormally expressed in this type of tumor and act as either tumor-suppressors or oncogenic RNAs (15,16). The abnormal expression of lncRNAs may contribute toward the malignancy of TScc by affecting a number of malignant characteristics (17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

Long non‑coding RNA PRNCR1 exerts oncogenic effects in�tongue squamous cell carcinoma in�vitro and in�vivo by sponging microRNA‑944 and thereby increasing HOXB5�expression

Zou

et al. 2020

Int J Mol Med

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A long non-coding RNA (lncRNA) called prostate cancer-associated non-coding RNA 1 (PRNCR1) serves crucial roles in the aggressive phenotypes of colorectal cancer and non-small cell lung cancer. However, there is little research on the expression profile, clinical value and detailed functions of PRNCR1 in tongue squamous cell carcinoma (TScc). The aim of the present study was to determine PRNCR1 expression in TScc and to examine the involvement of PRNCR1 in TScc progression. The molecular mechanisms behind the oncogenic effects of PRNCR1 in TScc cells were also investigated. PRNCR1 was revealed to be upregulated in TScc tumors and cell lines. The high PRNCR1 expression showed a significant correlation with tumor size, clinical stage, lymph node metastasis, and shorter overall survival times among patients with TScc. A PRNCR1-knockdown reduced TScc cell proliferation, migration and invasion, and increased apoptosis in vitro. Additionally, the PRNCR1-knockdown slowed down in vivo tumor growth of TScc cells. With regards to the mechanism, PRNCR1 acted as a competing endogenous RNA on microRNA-944 (miR-944) in TScc cells, and the effects of the PRNCR1-knockdown were reversed by an miR-944-knockdown. HOXB5 was validated as a direct target gene of miR-944 in TScc cells, and HOXB5 expression was found to be positively regulated by PRNCR1. Furthermore, resumption of HOXB5 expression reversed the tumor-suppressive actions of miR-944 in TScc cells. In conclusion, PRNCR1 acts as an oncogenic lncRNA in TScc through the upregulation of HOXB5 by sponging miR-944, thereby indicating a potential therapeutic target in TScc.

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Section: Introductionmentioning

confidence: 99%

Long non‑coding RNA PRNCR1 exerts oncogenic effects in�tongue squamous cell carcinoma in�vitro and in�vivo by sponging microRNA‑944 and thereby increasing HOXB5�expression

Zou

et al. 2020

Int J Mol Med

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“…The data are presented as the mean ± SD of three independent experiments. *P < 0.05; **P < 0.01. have been reported to regulate IGF2BP1 [35,36]. However, for the first time, we revealed the relationship between LINC00261 and IGF2BP1, providing a novel posttranscriptional mechanism for IGF2BP1 regulation.…”

Section: Discussionmentioning

confidence: 62%

Epigenetic silencing of LncRNA LINC00261 promotes c-myc-mediated aerobic glycolysis by regulating miR-222-3p/HIPK2/ERK axis and sequestering IGF2BP1

Zhai

Xie

et al. 2020

Oncogene

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Long noncoding RNAs have been identified as key regulators in the progression of various cancers. LINC00261 has been reported as a tumor suppressor in multiple cancers. However, its function and underlying mechanisms in pancreatic cancer remain largely unclear. Quantitative real-time PCR was performed to detect RNA expression. In situ hybridization was used to discover the subcellular location. The direct binding of LINC00261 to miR-222-3p was verified using a dual-luciferase reporter assay and RNA immunoprecipitation. LINC00261-binding proteins were detected using an RNA pulldown assay. LINC00261 was downregulated in pancreatic cancer tissues and cell lines. Its reduced expression was correlated with advanced pathological stage and poor prognosis. Forced expression of LINC00261 suppressed pancreatic cancer glycolysis and proliferation and induced cell cycle arrest and apoptosis. Mechanistically, downregulation of LINC00261 was caused by hypermethylation of the CpG island in the promoter region and EZH2-mediated histone H3 lysine 27 trimethylation. Moreover, LINC00261 exerted its biological function by binding to miR-222-3p to activate the HIPK2/ERK/c-myc pathway. In addition, LINC00261 could also reduce c-myc expression by sequestering IGF2BP1. Our study suggests that LINC00261 functions as a tumor suppressor in pancreatic cancer and identifies novel epigenetic and posttranscriptional regulatory mechanisms of LINC00261, which contribute to the targeted therapy of pancreatic cancer.

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“…IGF2BP1 belongs to RBPs that can bind to transcripts and regulate RNA stability. Predominantly expressed in the embryo, IGF2BP1 is an essential mediator through the interaction with RNAs in various cancers [25][26][27]. IGF2BP1 exerts synthesized effects, including cell proliferation, adhesion [28,29].…”

Section: Discussionmentioning

confidence: 99%

Molecular interplay between linc01134 and YY1 dictates hepatocellular carcinoma progression

Rong

Wang

et al. 2020

J Exp Clin Cancer Res

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Background: Revealing the mechanical role of long non-coding RNAs (lncRNAs) in tumorigenesis can contribute to novel therapeutic target for cancers. The regulatory role of linc01134 in hepatocellular carcinoma (HCC) has not been studied yet. Materials and methods: qRT-PCR and western blot were conducted to measure relevant RNA and protein expressions. CCK-8, colony formation, EdU, flow cytometry, wound-healing, transwell assays and xenograft experiments were performed to determine the role of linc01134 in HCC. ChIP and luciferase reporter assays were performed to analyze the effects of Yin Yang-1 (YY1) on linc01134 transcription activity. Relevant mechanical experiments were performed to verify interaction between relative genes. Results: YY1 enhanced linc01134 transcription by interacting with linc01134 promoter. Knockdown of linc01134 inhibited proliferation, migration and epithelial-mesenchymal transition (EMT), yet promoting apoptosis in HCC cells. Mechanically, linc01134 acted as miR-324-5p sponge and interacted with insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1) to increase the stability of YY1 mRNA expression. Up-regulated YY1 continuously stimulated linc01134 expression by enhancing linc01134 promoter activity, forming a positive feedback loop. Conclusion: Linc01134/miR-324-5p/IGF2BP1/YY1 feedback loop mediates HCC progression, which possibly provide prognosis and treatment target of HCC.

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LncRNA THOR promotes tongue squamous cell carcinomas by stabilizing IGF2BP1 downstream targets

Cited by 27 publications

References 34 publications

Long non‑coding RNA PRNCR1 exerts oncogenic effects in�tongue squamous cell carcinoma in�vitro and in�vivo by sponging microRNA‑944 and thereby increasing HOXB5�expression

Long non‑coding RNA PRNCR1 exerts oncogenic effects in�tongue squamous cell carcinoma in�vitro and in�vivo by sponging microRNA‑944 and thereby increasing HOXB5�expression

Epigenetic silencing of LncRNA LINC00261 promotes c-myc-mediated aerobic glycolysis by regulating miR-222-3p/HIPK2/ERK axis and sequestering IGF2BP1

Molecular interplay between linc01134 and YY1 dictates hepatocellular carcinoma progression

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