Silencing of Long Non-coding RNA MIAT Sensitizes Lung Cancer Cells to Gefitinib by Epigenetically Regulating miR-34a

Fu, Yunfeng; Li, Chengyuan; Luo, Yanwei; Li, Lian; Liu, Jing; Gui, Rong

doi:10.3389/fphar.2018.00082

Cited by 53 publications

(42 citation statements)

References 44 publications

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“…However, with respect to TSCC, no study has yet investigated the relationships between MIAT expression level and the prognosis of this disease. In our study, for the first time, we found that MIAT expression level TSCC specimen was significantly higher than that in adjacent nonneoplastic tongue tissue, this result was consistent with previous studies, 16,17 suggesting that MIAT was involved in the development of TSCC. In addition, correlation analysis showed that there is a significant positive correlation between MIAT levels in serum and MIAT was a risk factor for prognosis of TSCC within 12 months, whose high level means a poor prognosis of TSCC.…”

Section: Discussionsupporting

confidence: 93%

“…Li et al found that MIAT could interact with miR‐133, then promote the growth and invasion of pancreatic carcinoma cells, and indicate a poor prognosis. Study by Fu et al revealed that MIAT expression was associated with tumor size, lymph node metastasis, distant metastasis and TNM stage and was an independent factor for predicting the prognosis of lung cancer patients. However, with respect to TSCC, no study has yet investigated the relationships between MIAT expression level and the prognosis of this disease.…”

Section: Discussionmentioning

confidence: 99%

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Long non‐coding RNA myocardial infarction associated transcript promotes epithelial‐mesenchymal transition and is an independent risk factor for poor prognosis of tongue squamous cell carcinoma

Zhong

Wen

et al. 2019

J Oral Pathology Medicine

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Background Long non‐coding RNA myocardial infarction associated transcript (MIAT) has been suspected to be associated with poor prognosis in several malignancies. This study aims to investigate the association between MIAT expression levels and prognosis of tongue squamous cell carcinoma (TSCC). Materials and Methods Expressions of MIAT in TSCC specimens, corresponding adjacent non‐neoplastic tongue tissues, and serums collected from 116 TSCC patients were detected by Quantitative Real‐Time PCR. Then, these patients were followed up for 12 months after discharge. MIAT was suppressed and upregulated in TSCC cells, and then cell invasion and epithelial‐mesenchymal transition (EMT) markers were analyzed. Results Myocardial infarction associated transcript expression level in TSCC specimen was upregulated compared to adjacent non‐neoplastic tongue tissue and had a significant positive association with its level in serum. MIAT levels in both TSCC specimen and serum were correlated with cervical lymph node metastasis and histological grading of TSCC patients. Results of survival analysis showed that high expression levels of MIAT in both TSCC tissues and serums indicated higher mortality and shorter survival time of TSCC patients. Receiver operating characteristic curve analysis showed that there was no significant difference between MIAT in TSCC specimen and serum to differentiate death and non‐death of TSCC patients. In vitro study showed that MIAT could induce invasion of TSCC cells by regulating expressions of EMT markers through activation of Wnt/β‐catenin signaling pathway. Conclusion Upregulated MIAT promoted EMT of TSCC cells through activation of Wnt/β‐catenin signaling pathway and indicated a poor prognosis of TSCC, which may provide us a non‐invasive approach to evaluate the prognosis of TSCC.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Long non‐coding RNA myocardial infarction associated transcript promotes epithelial‐mesenchymal transition and is an independent risk factor for poor prognosis of tongue squamous cell carcinoma

Zhong

Wen

et al. 2019

J Oral Pathology Medicine

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“…Purified RNA was reverse transcribed into cDNA by using random primer with the QuantiTect Reverse Transcription Kit (Qiagen), and the presence of PAR5 transcripts was detected by qRT-PCR. Enrichment of PAR5 transcripts in the EZH2 immunoprecipitated lysate was calculated relative to the levels of PAR5 transcript in the rabbit IgG control sample, set equal to 1 [51,52].…”

Section: Rna Immunoprecipitation (Rip) Assaymentioning

confidence: 99%

The Long Non-Coding RNA Prader Willi/Angelman Region RNA5 (PAR5) Is Downregulated in Anaplastic Thyroid Carcinomas Where It Acts as a Tumor Suppressor by Reducing EZH2 Activity

Pellecchia

Sepe

Decaussin‐Petrucci

et al. 2020

Cancers

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Anaplastic thyroid carcinoma (ATC) represents one the most aggressive neoplasias in humans, and, nowadays, limited advances have been made to extend the survival and reduce the mortality of ATC. Thus, the identification of molecular mechanism underlying its progression is needed. Here, we evaluated the long non-coding RNA (lncRNA) expression profile of nine ATC in comparison with five normal thyroid tissues by a lncRNA microarray. By this analysis, we identified 19 upregulated and 28 downregulated lncRNAs with a fold change >1.1 or <−1.1 and p-value < 0.05, in ATC samples. Some of them were subsequently validated by qRT-PCR. Then, we investigated the role of the lncRNA Prader Willi/Angelman region RNA5 (PAR5), drastically and specifically downregulated in ATC. The restoration of PAR5 reduces proliferation and migration rates of ATC-derived cell lines indicating that its downregulation contributes to thyroid cancer progression. Our results suggest that PAR5 exerts its anti-oncogenic role by impairing Enhancer of Zeste Homolog 2 (EZH2) oncogenic activity since we demonstrated that PAR5 interacts with it in thyroid cancer cell lines, reducing EZH2 protein levels and its binding on the E-cadherin promoter, relieving E-cadherin from the negative regulation by EZH2. Consistently, EZH2 is overexpressed in ATC, but not in differentiated thyroid carcinomas. The results reported here define a tumor suppressor role for PAR5 in undifferentiated thyroid neoplasias, further highlighting the pivotal role of lncRNAs in thyroid carcinogenesis.

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“…Li et al found that MIAT contributed to the cell proliferation and metastasis of pancreatic carcinoma via interaction with miR‐133 . Fu et al demonstrated that MIAT was up‐regulated in lung cancer tissues and could sensitize lung cancer cells to gefitinib through epigenetically regulating miR‐34a . However, the function of MIAT in OS and the potential molecular mechanism are unknown.…”

Section: Introductionmentioning

confidence: 99%

LncRNA MIAT facilitates osteosarcoma progression by regulating mir‐128‐3p/VEGFC axis

et al. 2019

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The aberrant expression of long non‐coding RNAs (lncRNAs) has been involved in the progression of many human tumors including osteosarcoma (OS). However, the biological function and the underlying mechanism of the lncRNA myocardial infarction‐associated transcript (MIAT) in OS remain unclear. In the present study, we found that lncRNA MIAT was significantly up‐regulated in both OS tissues and cell lines, and high expression of MIAT was positively associated with tumor size and lymph node metastasis of OS patients. In addition, knockdown of MIAT inhibited proliferation, migration, invasion and promoted apoptosis of OS cells in vitro. Moreover, the expression of MIAT was negatively associated with miR‐128‐3p but positively correlated with vascular endothelial growth factor C (VEGFC) in OS. Further mechanistic study revealed that lncRNA MIAT promoted OS progression by up‐regulating VEGFC via sponging miR‐128‐3p in vitro. Taken together, our results suggest that MIAT/miR‐128‐3p/VEGFC axis contributes to OS progression and may be used as a novel therapeutic target for OS. © 2019 IUBMB Life, 9999(9999):1–9, 2019

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Silencing of Long Non-coding RNA MIAT Sensitizes Lung Cancer Cells to Gefitinib by Epigenetically Regulating miR-34a

Cited by 53 publications

References 44 publications

Long non‐coding RNA myocardial infarction associated transcript promotes epithelial‐mesenchymal transition and is an independent risk factor for poor prognosis of tongue squamous cell carcinoma

Long non‐coding RNA myocardial infarction associated transcript promotes epithelial‐mesenchymal transition and is an independent risk factor for poor prognosis of tongue squamous cell carcinoma

The Long Non-Coding RNA Prader Willi/Angelman Region RNA5 (PAR5) Is Downregulated in Anaplastic Thyroid Carcinomas Where It Acts as a Tumor Suppressor by Reducing EZH2 Activity

LncRNA MIAT facilitates osteosarcoma progression by regulating mir‐128‐3p/VEGFC axis

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