The long noncoding RNA HULC promotes liver cancer by increasing the expression of the HMGA2 oncogene via sequestration of the microRNA-186

Wang, Yuan; Chen, Fuquan; Zhao, Man; Yang, Zhe; Li, Jiong; Zhang, Shuqin; Zhang, Weiying; Ye, Lihong; Zhang, Xiaodong

doi:10.1074/jbc.m117.783738

Cited by 123 publications

(97 citation statements)

References 49 publications

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“…Moreover, aberrant expression of ncRNAs has been documented in several human tumors, suggesting that ncRNAs may significantly contribute to their pathogenesis . For example, lncRNA‐HULC overexpression may suppress miR‐186 expression, resulting in increased expression of its target protein, HMGA2, which serves as an oncogene in hepatocellular carcinoma . Such mRNA/miR‐lncRNA coregulatory pairs (eg, TCF7L2/miR‐217‐CRNDE and TUSC7/miR‐211‐CDK6) have also been demonstrated in CRC …”

Section: Introductionmentioning

confidence: 99%

Small nucleolar RNA host gene 1 promotes development and progression of colorectal cancer through negative regulation of miR‐137

Yin

Peng

et al. 2019

Molecular Carcinogenesis

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Small nucleolar RNA host gene 1 (SNHG1) is critical in the progression of cancers. However, the mechanism by which SNHG1 regulates the progression of colorectal cancer (CRC) remains unclear. Expressions of SNHG1 and miR‐137 in CRC tissues and cell lines were evaluated by quantitative real‐time polymerase chain reaction. A luciferase reporter gene assay was conducted to investigate miR‐137 target. Additionally, RNA pull‐down assay was performed to explore the physical association between miR‐137, SNHG1, and RNA induced silencing complex (RISC). Cell cycling and invasion were examined by flow cytometry (FCM) and transwell assays. The in vivo carcinogenic activity of SNHG1 was examined using murine xenograft models. Expression of RICTOR, serine/threonine kinase 1 (AKT), serum and glucocorticoid‐inducible kinase 1 (SGK1), p70S6K1, and LC3II/LC3I ratio was examined by Western blot analysis. SNHG1 upregulation was observed in CRC tissues and cell lines, which was associated with the lymph node metastasis, advanced TNM stage and poorer prognosis. SNHG1 increased RICTOR level in CRC via sponging miR‐137. In addition, SNHG1 silencing inhibited CRC cell proliferation and migration in vitro and in vivo. SNHG1 regulated RICTOR expression by sponging miR‐137 and promoted tumorgenesis in CRC.

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Section: Introductionmentioning

confidence: 99%

Small nucleolar RNA host gene 1 promotes development and progression of colorectal cancer through negative regulation of miR‐137

Yin

Peng

et al. 2019

Molecular Carcinogenesis

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“…STAT3‐NF‐κB‐fascin signaling pathway is indicated as a target for inhibiting GC development (Yao et al, ). Gankyrin can promote EMT process and metastasis in NSCLC via activating IL‐6/STAT3 signaling pathway (Wang, Chen, et al, ).…”

Section: Introductionmentioning

confidence: 99%

H19 promotes non‐small‐cell lung cancer (NSCLC) development through STAT3 signaling via sponging miR‐17

Huang

Lei

et al. 2018

Journal Cellular Physiology

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LncRNAs can exhibit crucial roles in the development of multiple cancers, including non-small cell lung cancer (NSCLC). Currently, we investigated the role of lncRNA H19 in NSCLC. In our study, it was found that H19 was upregulated in A549 and H1299 cells compared to normal lung epithelial BEAS-2B cells. Meanwhile, we observed that miR-17 was downregulated in NSCLC cell lines. Inhibited H19 can suppress the growth, migration, and invasion of NSCLC cells and bioinformatics search was performed to predict the correlation between H19 and miR-17. Overexpression of miR-17 was able to inhibit the progression of NSCLC cells while reversely miR-17 inhibitors reversed this process. In addition, signal transducers and activators of transcription (STAT3), as an mRNA target of miR-17, was presented in our research. Moreover, we discovered that H19 demonstrated its biological functions via regulating miR-17 and STAT3 in vitro. Silencing H19 greatly increased STAT3 expression by sponging miR-19 in vitro. It was hypothesized that H19 may serve as a competing endogenous RNA (ceRNA) to modulate STAT3 by attaching miR-17 in lung cancer. In summary, our findings indicated that H19/miR-17/STAT3 axis participated in NSCLC development. H19 could be regarded as a significant prognostic biomarker in NSCLC progression.

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“…However, such therapy will likely be challenged by the mode of delivery to the intended organ, tissue, and cells, as well as by potential off-target effects. Like the interactions between miRNAs and mRNAs, the interactions between lncRNAs and miRNAs have been reported in the pathogenesis of several cancers, including OC [94,95], gastric [96], hepatocellular carcinoma [97]. Understanding of the interactions between lncRNAs and miRNAs, and their subsequent impacts on the target molecules may facilitate an immense use of lncRNAs as therapeutic targets in future therapies.…”

Section: Targeting Lncrna and Mirna Network For Therapeutic Developmentmentioning

confidence: 99%

Long Non-Coding RNAs: the New Horizon of Gene Regulation in Ovarian Cancer

Worku

Bhattarai

Ayers

et al. 2017

Cell Physiol Biochem

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Long non-coding RNAs (lncRNAs), a class of non-coding transcripts, have recently been emerging with heterogeneous molecular actions, adding a new layer of complexity to generegulation networks in tumorigenesis. LncRNAs are considered important factors in several ovarian cancer histotypes, although few have been identified and characterized. Owing to their complexity and the lack of adapted molecular technology, the roles of most lncRNAs remain mysterious. Some lncRNAs have been reported to play functional roles in ovarian cancer and can be used as classifiers for personalized medicine. The intrinsic features of lncRNAs govern their various molecular mechanisms and provide a wide range of platforms to design different therapeutic strategies for treating cancer at a particular stage. Although we are only beginning to understand the functions of lncRNAs and their interactions with microRNAs (miRNAs) and proteins, the expanding literature indicates that lncRNA-miRNA interactions could be useful biomarkers and therapeutic targets for ovarian cancer. In this review, we discuss the genetic variants of lncRNAs, heterogeneous mechanisms of actions of lncRNAs in ovarian cancer tumorigenesis, and drug resistance. We also highlight the recent developments in using lncRNAs as potential prognostic and diagnostic biomarkers. Lastly, we discuss potential approaches for linking lncRNAs to future gene therapies, and highlight future directions in the field of ovarian cancer research.

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The long noncoding RNA HULC promotes liver cancer by increasing the expression of the HMGA2 oncogene via sequestration of the microRNA-186

Cited by 123 publications

References 49 publications

Small nucleolar RNA host gene 1 promotes development and progression of colorectal cancer through negative regulation of miR‐137

Small nucleolar RNA host gene 1 promotes development and progression of colorectal cancer through negative regulation of miR‐137

H19 promotes non‐small‐cell lung cancer (NSCLC) development through STAT3 signaling via sponging miR‐17

Long Non-Coding RNAs: the New Horizon of Gene Regulation in Ovarian Cancer

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