Long noncoding RNA HULC modulates the phosphorylation of YB‐1 through serving as a scaffold of extracellular signal–regulated kinase and YB‐1 to enhance hepatocarcinogenesis

Li, Dan; Li, Xuefeng; Zhou, Jian; Hu, Jie; Zhang, Dongdong; Liu, Jing; Qiao, Yanyan; Zhan, Qimin

doi:10.1002/hep.29010

Cited by 171 publications

(139 citation statements)

References 50 publications

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“…Combining RNA pull-down assays and mass spectrometry analysis, we identified YBX1 as a specific lncRNA-AWPPH interacting protein. YBX1 is a highly conserved and multifunctional protein, which binds both DNA and RNA, participates in transcription regulation, RNA processing and translation regulation, and plays pro-oncogenic roles in tumor progression, metastasis, and drug resistance in various cancers [42][43][44][45][46].…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA AWPPH promotes hepatocellular carcinoma progression through YBX1 and serves as a prognostic biomarker

Zhao

Liu

2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

100

107

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Long noncoding RNAs (lncRNAs) have been shown to play important roles in various cancers. However, the clinical significances and biological roles of lncRNAs in hepatocellular carcinoma (HCC) remain largely unknown. In this study, using online-available data sets and quantitative real-time PCR, we identified a novel lncRNA termed lncRNA-AWPPH, which is highly expressed in HCC tissues. Its upregulation is correlated with encapsulation incomplete, microvascular invasion, advanced TNM stage and BCLC stage. Cox proportional hazards regression analysis revealed that high lncRNA-AWPPH expression is an independent prognostic factor for poor recurrence-free and overall survival. Functional experiments showed that overexpression of lncRNA-AWPPH promotes HCC cell proliferation and migration in vitro, and tumor growth and metastasis in vivo. Conversely, depletion of lncRNA-AWPPH has opposite effects on HCC. Mechanistically, lncRNA-AWPPH interacts with YBX1, promotes YBX1-mediated activation of SNAIL1 translation, and upregulates SNAIL1 expression. Furthermore, lncRNA-AWPPH promotes YBX1-mediated activation of PIK3CA transcription, upregulates PIK3CA expression, and activates PI3K/AKT pathway. Depletion of YBX1 abolishes the effects of lncRNA-AWPPH on SNAIL1 and PIK3CA, and also the biological roles of lncRNA-AWPPH on HCC cells. In conclusion, this study identifies a novel lncRNA termed lncRNA-AWPPH which is highly expressed in HCC, indicates poor prognosis of HCC patients, and promotes HCC cell proliferation, migration, and in vivo tumor growth and metastasis via a novel regulatory mechanism of interacting with YBX1.

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Section: Discussionmentioning

confidence: 99%

Long noncoding RNA AWPPH promotes hepatocellular carcinoma progression through YBX1 and serves as a prognostic biomarker

Zhao

Liu

2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

100

107

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“…Deregulated lncRNAs have been reported to be associated with the tumorigenesis and metastasis of HCC [5]. For example, lnc-EGFR accelerates T-regulatory cell differentiation leading to immune evasion of HCC [6], and a variety of lncRNAs, such as MALT1 [7], TP73-AS1 [8], HULC [9], XIST [10], and HOTAIR [11], function as oncogenes, promoting HCC growth and metastasis by regulating miRNA or proteins. However, lncRNA uc.134 and lincRNA-p21 inhibit HCC progression by repressing CUL4A-mediated ubiquitination of LATS1 [12] or activating endoplasmic reticulum stress [13].…”

Section: Introductionmentioning

confidence: 99%

lncRNA SNHG8 Promotes the Tumorigenesis and Metastasis by Sponging miR-149-5p and Predicts Tumor Recurrence in Hepatocellular Carcinoma

Dong

Teng

Guo

et al. 2018

Cell Physiol Biochem

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Background/Aims: Long noncoding RNAs (lncRNAs) are aberrantly expressed in multiple malignant tumors involved in tumor growth and metastasis. Accumulating data show that small nucleolar RNA host gene (SNHG) 1/12/20 plays a key role in the progression of hepatocellular carcinoma (HCC). However, the molecular mechanisms by which SNHG8 contributes to HCC remain elusive and merit exploration. Methods: The association between SNHG8 expression and the clinicopathological characteristics and prognoses in HCC patients was analysed by using qRT-PCR analysis and the data from The Cancer Genome Atlas. Cell growth and metastatic potential were determined by MTT, colony formation, Transwell assays, and the mouse xenograft tumor model and lung metastasis model. Epithelial–mesenchymal transition markers were detected by western blot analysis. The binding capacity of SNHG8 with miRNAs was evidenced by bioinformatic analysis and a luciferase reporter assay. In addition, the rescue experiments were performed based on co-transfection with sh-SNHG8 and a miR-149 inhibitor in HCC cells. Results: The expression levels of lncRNA SNHG8 were dramatically increased in HCC tissues and cell lines as compared with the adjacent normal tissues, and SNHG8 expression was an independent prognostic factor of tumor recurrence in HCC patients. Furthermore, knockdown of SNHG8 inhibited cell proliferation, invasion, and lung metastasis in vitro and in vivo, whereas overexpression of SNHG8 reversed these effects. SNHG8 acted as a sponge of miR-149 and counteracted the tumor suppressive effects of mi R-149 in HCC cells. Expression of phosphatase, Mg2+/Mn2+ dependent 1F, a target of R-149, displayed a negative correlation with miR-149 expression but a positive correlation with SNHG8 expression in HCC specimens. Conclusion: As lncRNA SNHG8 may promote HCC tumorigenesis and metastasis by sponging miR-149, it is a potential candidate marker and therapeutic target for HCC.

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“…The aberrant expression of lncRNAs in various cancers has attracted attention, and the biological functions of lncRNAs are increasingly being shown. LncRNA HULC (highly upregulated in liver cancer) was found to be upregulated in hepatocarcinoma, regulating phosphorylation of Y‐box binding proteins and increasing translation of some oncogenic mRNAs . DSCAM‐AS1 was reported to mediate BC development and drug resistance by heterogeneous nuclear ribonucleoprotein L protein .…”

Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA‐CTD‐2108O9.1 represses breast cancer metastasis by influencing leukemia inhibitory factor receptor

Wang

et al. 2018

Cancer Science

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Breast cancer (BC) is an aggressive malignant disease in women worldwide with a high tendency to metastasize. However, important biomarkers for BC metastasis remain largely undefined. In the present study, we identified that long non‐coding RNA‐CTD‐2108O9.1 is downregulated in BC tissues and cells and acts as a metastatic inhibitor of BC. Mechanistic investigation determined that lncRNA‐CTD‐2108O9.1 represses metastasis by targeting leukemia inhibitory factor receptor (LIFR), which is designated as a metastasis suppressor in BC. Our study characterizes a significant tumor suppressor active in BC metastasis repression through the known metastasis inhibitor LIFR.

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Long noncoding RNA HULC modulates the phosphorylation of YB‐1 through serving as a scaffold of extracellular signal–regulated kinase and YB‐1 to enhance hepatocarcinogenesis

Cited by 171 publications

References 50 publications

Long noncoding RNA AWPPH promotes hepatocellular carcinoma progression through YBX1 and serves as a prognostic biomarker

Long noncoding RNA AWPPH promotes hepatocellular carcinoma progression through YBX1 and serves as a prognostic biomarker

lncRNA SNHG8 Promotes the Tumorigenesis and Metastasis by Sponging miR-149-5p and Predicts Tumor Recurrence in Hepatocellular Carcinoma

Long non‐coding RNA‐CTD‐2108O9.1 represses breast cancer metastasis by influencing leukemia inhibitory factor receptor

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