EMT-related long non-coding RNA in hepatocellular carcinoma: A study with TCGA database

Zong-lin, Zhang; Wang, Surong; Liu, Wenqi

doi:10.1016/j.bbrc.2018.07.075

Cited by 30 publications

(25 citation statements)

References 33 publications

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“…The next step incorporated the assessment of the effect of MIAT downregulation on cell migration, as implicated by the sequencing results. Similarly to our sequencing, prior functional annotation had implied that MIAT is associated with EMT-related canonical pathways in hepatocellular carcinoma cells [47], including the TGF-β pathway, justifying the perturbations in this pathway following the perturbation in MIAT expression in our study. Furthermore, consistent with other studies reporting that MIAT is involved in cell migration and invasion and its downregulation inhibits this effect in other cancer types, for example in NSCLC (non-small-cell lung cancer) [48], colorectal cancer [49], clear cell renal cell carcinoma [50] and breast cancer [51], our results reveal that the ability of neuroblastoma and GBM cells to migrate is as well inhibited to an important extent when MIAT is knocked down.…”

Section: Discussionsupporting

confidence: 63%

RNA sequencing reveals a key role for the long non-coding RNA MIAT in regulating neuroblastoma and glioblastoma cell fate

Bountali

Tonge

Mourtada-Maarabouni

2019

International Journal of Biological Macromolecules

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Myocardial Infraction Associated Transcript (MIAT) is a subnuclear lncRNA that interferes with alternative splicing and is associated with increased risk of various heart conditions and nervous system tumours. The current study aims to elucidate the role of MIAT in cell survival, apoptosis and migration in neuroblastoma and glioblastoma multiforme. To this end, MIAT was silenced by MIAT-specific siRNAs in neuroblastoma and glioblastoma cell lines, and RNA sequencing together with a series of functional assays were performed. The RNA sequencing has revealed that the expression of an outstanding number of genes is altered, including genes involved in cancer-related processes, such as cell growth and survival, apoptosis, reactive oxygen species (ROS) production and migration. Furthermore, the functional studies have confirmed the RNA sequencing leads, with our key findings suggesting that MIAT knockdown eliminates long-term survival and migration and increases basal apoptosis in neuroblastoma and glioblastoma cell lines. Taken together with the recent demonstration of the involvement of MIAT in glioblastoma, our observations suggest that MIAT could possess tumour-promoting properties, thereby acting as an oncogene, and has the potential to be used as a reliable biomarker for neuroblastoma and glioblastoma and be employed for prognostic, predictive and, potentially, therapeutic purposes for these cancers.

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Section: Discussionsupporting

confidence: 63%

RNA sequencing reveals a key role for the long non-coding RNA MIAT in regulating neuroblastoma and glioblastoma cell fate

Bountali

Tonge

Mourtada-Maarabouni

2019

International Journal of Biological Macromolecules

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“…15 However, Meg3 contributes to the EMT phenotype, migration and invasion of HCC (Hepatocellular carcinoma) cells. 16 Nevertheless, the role of Meg3 in EMT and invasion has not been well explored in glioma cells.…”

Section: Introductionmentioning

confidence: 99%

<p>Meg3 Induces EMT and Invasion of Glioma Cells via Autophagy</p>

Yang

Bian

et al. 2020

OTT

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Background: Glioma is one of the most common malignant tumors. Glioblastoma (grade IV) is considered the most malignant form of human brain tumors. Maternal expression gene 3 (Meg3) encodes a non-coding RNA (ncRNA) that plays an important role in the development and progression of cancer. However, the role of Meg3 in glioma cells remains largely unclear. Methods: Reverse transcription-quantitative (RT-q) PCR was conducted to evaluate the mRNA expression related to cell autophagy and EMT while protein expression was detected by Western blotting. Staining of acidic vacuoles and immunofluorescence staining were used to detect autophagy. The ability of cells to migrate and invade was detected by Transwell migration and invasion assays. Results: In the present study, it was found that the overexpression of Meg3 induced EMT, migration and invasion of glioma cells, whereas Meg3 overexpression induced autophagy of glioma cells. More importantly, the inhibition of autophagy impaired the EMT of glioma cells. In addition, Meg3-induced EMT, migration and invasion could be partially reversed by autophagy inhibitors, chloroquine (CQ) and Lys05, in glioma cells. Conclusion: All data suggest that Meg3 induces EMT and invasion of glioma cells via autophagy. Overall, the findings of the present study demonstrate the importance of Meg3 in the molecular etiology of glioma, which also indicate its potential applications in the treatment of glioma.

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“…Originally, oxidative stress and cyclic mechanical stress induced the dysregulation of LOXL1-AS1 expression in human lens epithelial cells and human Schlemm's canal endothelial cells respectively [11]. Afterward, the role of LOXL1-AS1 has been investigated in several types of human cancer including lung cancer [12], hepatocellular carcinoma [13], glioma [14,15], breast cancer [16,17], prostate cancer [18], and medulloblastoma [19]. However, the expression pattern and function of LOXL1-AS1 in osteosarcoma is still unknown.…”

Section: Introductionmentioning

confidence: 99%

LOXL1-AS1 predicts poor prognosis and promotes cell proliferation, migration, and invasion in osteosarcoma

Chen

2019

Bioscience Reports

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lncRNA LOXL1 antisense RNA 1 (lncRNA LOXL1-AS1) was recently found to function as oncogenic lncRNA in glioblastoma, prostate cancer, and medulloblastoma. The role of LOXL1-AS1 in osteosarcoma was still unknown. In our study, we found LOXL1-AS1 expression levels were higher in osteosarcoma tissues and cell lines than normal bone tissues and normal osteoblast cell line, respectively. Moreover, high-expression of LOXL1-AS1 was correlated with Enneking stage, tumor size, distant metastasis, histological grade, and overall survival time in osteosarcoma patients. Furthermore, LOXL1-AS1 overexpression acted as an independent poor predictor for overall survival in osteosarcoma patients. The loss-of-function studies showed knockdown of LOXL1-AS1 dramatically inhibited osteosarcoma cell proliferation, migration, and invasion through suppressing PI3K-AKT pathway. In conclusion, LOXL1-AS1 predicts clinical progression and poor prognosis in osteosarcoma patients and functions as oncogenic lncRNA to regulate cell proliferation, cell cycle, migration, and invasion.

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EMT-related long non-coding RNA in hepatocellular carcinoma: A study with TCGA database

Cited by 30 publications

References 33 publications

RNA sequencing reveals a key role for the long non-coding RNA MIAT in regulating neuroblastoma and glioblastoma cell fate

RNA sequencing reveals a key role for the long non-coding RNA MIAT in regulating neuroblastoma and glioblastoma cell fate

<p>Meg3 Induces EMT and Invasion of Glioma Cells via Autophagy</p>

LOXL1-AS1 predicts poor prognosis and promotes cell proliferation, migration, and invasion in osteosarcoma

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