Overexpression of Long Non-coding RNA HOTAIR Predicts Tumor Recurrence in Hepatocellular Carcinoma Patients Following Liver Transplantation

Yang, Zhe; Zhou, Lin; Wu, Liming; Lai, Ming-Chun; Xie, Haiyang; zhang, Feng; Zheng, Shusen

doi:10.1245/s10434-011-1581-y

Cited by 647 publications

(573 citation statements)

References 20 publications

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“…16,17 Accumulating studies have indicated that HOTAIR is upregulated in cancers including HCC. [18][19][20] It has been reported that HOTAIR regulates gene expression via epigenetic modifications. 21 For example, Rinn et al demonstrated that HOTAIR interacts with polycomb-repressive complex 2 (PRC2) to increase the trimethylation of histone H3 lysine-27 (H3K27), resulting in the reduction of HOXD gene expression.…”

Section: Introductionmentioning

confidence: 99%

HOTAIR Epigenetically Modulates PTEN Expression via MicroRNA-29b: A Novel Mechanism in Regulation of Liver Fibrosis

et al. 2017

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Section: Introductionmentioning

confidence: 99%

HOTAIR Epigenetically Modulates PTEN Expression via MicroRNA-29b: A Novel Mechanism in Regulation of Liver Fibrosis

et al. 2017

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“…11,16 In fact, previous studies have shown that particular deregulated lncRNAs are important regulators of tumor formation and progression. 17,24 For example, the antisense intergenic RNA HOX Antisense Intergenic RNA (HOTAIR) is highly expressed in multiple types of primary somatic tumors, such as hepatocellular carcinoma, 25,26 pancreatic cancer, 27 and gastric cancer, 28 as well as some metastatic tumors, including metastatic breast tumors 29 and melanoma. 30 Moreover, high HOTAIR level is associated with poor patient survival rate 20,27 and tumor recurrence.…”

Section: Lncrnas In Cancermentioning

confidence: 99%

“…30 Moreover, high HOTAIR level is associated with poor patient survival rate 20,27 and tumor recurrence. 25 It was discovered that HOTAIR represses transcription across 40 kb of the HOXD locus by acting as a scaffold of histone modification complexes; it binds with polycomb chromatin remodeling complexes in trans, which lead to alterations of cells' epigenetic state and subsequent gene expression. 31 Moreover, HOTAIR can also interact with the LSD1/CoREST/REST complex, which coordinates targeting of LSD1 to chromatin for coupled histone K4 demethylation.…”

Section: Lncrnas In Cancermentioning

confidence: 99%

“…31 Moreover, HOTAIR can also interact with the LSD1/CoREST/REST complex, which coordinates targeting of LSD1 to chromatin for coupled histone K4 demethylation. 32 Given its important role in the epigenetic regulation of gene expression by mediating the modulation of chromatin structures, it is not surprising that HOTAIR performs vital functions in increasing cancer invasiveness and metastasis 25,26,29 and shows immense clinical relevance. Particularly, lncRNA expression levels may be extremely useful for monitoring tumors, and we consider lncRNAs to be novel cancer diagnostic tools and a source of future therapies.…”

Section: Lncrnas In Cancermentioning

confidence: 99%

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Long non-coding RNAs in colorectal cancer: implications for pathogenesis and clinical application

Pan

2014

Modern Pathology

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Long non-coding RNAs (lncRNAs) are a class of newly identified non-coding RNA molecules that are emerging as key regulators of tumor initiation and development. Colorectal cancer (CRC) remains a major health problem worldwide, and there remains a need to further refine the current screening approaches as well as provide tailored diagnostic and therapeutic approaches. Multiple dysregulated lncRNAs participate in tumorigenesis through a variety of molecular mechanisms, and various regulatory factors frequently contribute to the aberrant expression of lncRNAs in CRC, thereby allowing malignant transformation. Additionally, the association of dysregulated lncRNAs with specific developmental stages and clinical outcomes indicates their potential as strong diagnostic and prognostic predictors as well as therapeutic targets. Here we provide a brief overview of the known functions of CRC-associated lncRNAs, describe some potential molecular mechanisms that underlie changes in lncRNA expression in CRC, and attempt to uncover their clinical and therapeutic potential. Keywords: colorectal cancer; diagnosis; dysregulation; long non-coding RNA; prognosis High-throughput genome-scale studies have demonstrated that more than 93% of the DNA sequences in the human genome are actively transcribed. 1 However, only approximately 5-10% of the sequences are stably transcribed into mRNA or non-coding RNA (ncRNA). Genome tiling arrays have revealed that the amount of non-coding sequence is at least four times larger than the amount of coding sequence, which indicates that only 1% of the human genome is composed of protein-coding genes and the remaining 4-9% is transcribed into ncRNAs. 2 Therefore, ncRNAs constitute a very large proportion of the total RNA molecules.The function and clinical significance of short regulatory ncRNAs, such as microRNAs (miRNAs) and small interfering RNAs (siRNAs), were elucidated first, 3 and the regulatory roles of miRNAs have been broadly recognized in almost all physiological and pathological processes in the body, including carcinogenesis. 4 For example, we previously reported that MIR95 promotes cell proliferation and targets sorting nexin 1 in human colorectal carcinoma; 5 moreover, in colorectal cancer (CRC) patients, the plasma levels of MIR29a and MIR92a are significantly upregulated and the plasma levels of MIR601 and MIR760 are significantly downregulated; thus the levels of these miRNAs have good diagnostic value for CRC screening. 6,7 According to their transcript size, ncRNAs are grouped into two major classes: (i) small ncRNAs with transcripts o200 nucleotides (nt; eg, aforementioned siRNAs and miRNAs, Piwi-interacting RNAs, and some retrotransposon-derived RNAs) and (ii) long non-coding RNAs (lncRNAs), this class includes five broad categories: sense, antisense, bidirectional, intronic, and intergenic, based on the proximity between neighboring transcripts. 8 For a time, lncRNAs was commonly defined as a proteincoding transcripts that is 4200 nt. 9 However, this definition is arbitrary and ...

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“…Of note, a microarray analysis confirmed that lncRNAs HOX antisense intergenic RNA (HOAIR), CCAT1 and HIF1A‐AS1 were over‐expressed within retinoblastoma tissues, yet lncRNAs MIR31HG, BCAR4 and H193 were evidently under‐expressed within retinoblastoma tissues 13. Among them, HOTAIR was identified to be a cis‐acting parameter within the HOXC loca,14, 15, 16 and its carcinogenicity has been authenticated within breast cancer, liver cancer, colorectal cancer, oesophageal squamous cancer, pancreatic cancer, non‐small cell lung cancer and cervical cancer 17, 18, 19, 20, 21, 22, 23, 24. In addition, HOAIR was indicated as a potential therapeutic biomarker for retinoblastoma, and silencing of HOTAIR could attenuated proliferation, migration and invasion of retinoblastoma cells were determined after 25…”

Section: Introductionmentioning

confidence: 99%

LncRNA HOTAIR/miR‐613/c‐met axis modulated epithelial‐mesenchymal transition of retinoblastoma cells

Yang

et al. 2018

J Cellular Molecular Medi

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Since lncRNAs could modulate neoplastic development by modulating downstream miRNAs and genes, this study was carried out to figure out the synthetic contribution of HOTAIR, miR‐613 and c‐met to viability, apoptosis and proliferation of retinoblastoma cells. Totally 276 retinoblastoma tissues and tumour‐adjacent tissues were collected, and human retinoblastoma cell lines (ie, Y79, HXO‐Rb44, SO‐Rb50 and WERI‐RB1) were also gathered. Moreover, transfections of pcDNA3.1‐HOTAIR, si‐HOTAIR, miR‐613 mimic, miR‐613 inhibitor, pcDNA3.1/c‐met were performed to evaluate the influence of HOTAIR, miR‐613 and c‐met on viability, apoptosis and epithelial‐mesenchymal transition (EMT) of retinoblastoma cells. Dual‐luciferase reporter gene assay was also arranged to confirm the targeted relationship between HOTAIR and miR‐613, as well as between miR‐613 and c‐met. Consequently, up‐regulated HOTAIR and down‐regulated miR‐613 expressions displayed associations with poor survival status of retinoblastoma patients (P < 0.05). Besides, inhibited HOTAIR and promoted miR‐613 elevated E‐cadherin expression, yet decreased Snail and Vimentin expressions (P < 0.05). Simultaneously, cell proliferation and cell viability were also less‐motivated (P < 0.05). Nonetheless, c‐met prohibited the functioning of miR‐613, resulting in promoted cell proliferation and viability, along with inhibited cell apoptosis (P < 0.05). Finally, HOTAIR was verified to directly target miR‐613, and c‐met was the direct target gene of miR‐613 (P < 0.05). In conclusion, the role of lncRNA HOTAIR/miR‐613/c‐met signalling axis in modulating retinoblastoma cells’ viability, apoptosis and expressions of EMT‐specific proteins might provide evidences for developing appropriate diagnostic and treatment strategies for retinoblastoma.

show abstract

Overexpression of Long Non-coding RNA HOTAIR Predicts Tumor Recurrence in Hepatocellular Carcinoma Patients Following Liver Transplantation

Abstract: The high expression level of HOTAIR in HCC could be a candidate biomarker for predicting tumor recurrence in HCC patients who have undergone liver transplant therapy and might be a potential therapeutic target.

Cited by 647 publications

References 20 publications

HOTAIR Epigenetically Modulates PTEN Expression via MicroRNA-29b: A Novel Mechanism in Regulation of Liver Fibrosis

HOTAIR Epigenetically Modulates PTEN Expression via MicroRNA-29b: A Novel Mechanism in Regulation of Liver Fibrosis

Long non-coding RNAs in colorectal cancer: implications for pathogenesis and clinical application

LncRNA HOTAIR/miR‐613/c‐met axis modulated epithelial‐mesenchymal transition of retinoblastoma cells

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