MiR-598: A tumor suppressor with biomarker significance in osteosarcoma

Liu, Kai; Sun, Xiaolu; Zhang, Yingang; Liu, Liang; Yuan, Qiling

doi:10.1016/j.lfs.2017.09.003

Cited by 33 publications

(29 citation statements)

References 31 publications

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“…miR-598 expression is also downregulated in osteosarcoma tissues, serum and cell lines. miR-598 directly targets PDGFB and MET to serve as a tumor suppressor in osteosarcoma by regulating cell proliferation, migration, invasion, and apoptosis in vitro, as well as tumor growth in vivo (21). A study by Chen et al (22) reported that miR-598 is lowly expressed in colorectal cancer.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA‑598 inhibits the proliferation and invasion of non‑small cell lung cancer cells by directly targeting ZEB2

Tong

Huang

et al. 2018

Exp Ther Med

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An increasing number of studies have observed that microRNAs (miRNAs) are abnormally expressed in non-small cell lung cancer (NSCLC), and that their aberrant expression links with the progression and development of NSCLC. Therefore, it is necessary to full elucidate the specific roles of miRNAs in NSCLC, as this may facilitate the identification of novel therapeutic targets. In the present study, it was observed that miRNA-598 (miR-598) expression was significantly downregulated in NSCLC tissues and cell lines. Decreased miR-598 was negatively correlated with TNM stage and lymph node metastasis in NSCLC patients. In addition, ectopic expression of miR-598 reduced NSCLC cell proliferation and invasion in vitro. The zinc finger E-box-binding homeobox 2 (ZEB2) was validated as a direct target of miR-598 in NSCLC cells. ZEB2 was upregulated in NSCLC tissues and the upregulation of ZEB2 was inversely correlated with the miR-598 level. The results revealed that restored ZEB2 expression abrogated the inhibitory effects of miR-598 overexpression in NSCLC cells. In conclusion, the results of the present study revealed that miR-598 may inhibit the progression of NSCLC by directly targeting ZEB2, which suggests that this miRNA may be identified as a potential novel prognostic biomarker and therapeutic target for patients with NSCLC.

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Section: Discussionmentioning

confidence: 99%

“…It has been reported that miR-598 implicates in the initiation and progression of several human cancers (20)(21)(22). However, the expression and functions of miR-598 in NSCLC as well as its potential regulatory mechanisms are still unknown.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‑598 inhibits the proliferation and invasion of non‑small cell lung cancer cells by directly targeting ZEB2

Tong

Huang

et al. 2018

Exp Ther Med

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“…Presently, several studies have explored the role of miR-598 in the development of various cancers. The overexpression of miR-598 suppressed the proliferation, migration, and invasion of osteosarcoma cells [13]. Moreover, miR-598 always inhibits EMT and suppresses metastasis in colorectal cancer by targeting JAG1 [14].…”

Section: Discussionmentioning

confidence: 99%

“…Recently, Liu et al . reported that miR-598 acts as a tumor suppressor in the proliferation, migration, and invasion of osteosarcoma cells [13]. Another study by Chen et al .…”

Section: Introductionmentioning

confidence: 99%

MiR-598 Suppresses Invasion and Migration by Negative Regulation of Derlin-1 and Epithelial-Mesenchymal Transition in Non-Small Cell Lung Cancer

Yang

Wei

Qin

et al. 2018

Cell Physiol Biochem

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Background/Aims: MicroRNAs regulate a wide range of biological processes of non-small cell lung cancer (NSCLC). Although miR-598 has been reported to act as a suppressor in osteosarcoma and colorectal cancer, the physiological function of miR-598 in NSCLC remains unknown. In this study, the role of miR-598 in NSCLC was investigated. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to estimate the expression of miR-598 and Derlin-1 (DERL1) in both NSCLC tissues and cell lines. Immunohistochemistry (IHC) analyzed the association between the miR-598 expression and epithelial-mesenchymal transition (EMT) hallmark genes (E-cadherin, Vimentin) by staining the tumors representative of the high- and low-expression groups. The effect of miR-598 and DERL1 on invasion and migration was determined in vitro using transwell and wound-healing assays. The molecular mechanism underlying the relevance between miR-598 and DERL1 was elucidated by luciferase assay and Western blot. Western blot assessed the expression levels of EMT hallmark genes in cell lines. Xenograft tumor formation assay was conducted as an in vivo experiment. Results: In this study, a relatively low level of miR-598 and high DERL1 expressions were found in NSCLC specimens and cell lines. IHC results established a positive correlation between the miR-598 expression and E-cadherin and a negative with Vimentin. DERL1 was verified as a direct target of miR-598 by luciferase assay. In vitro, the over-expression of miR-598 negatively regulated DERL1 and EMT for the suppression of invasion and migration. In vivo, the over-expression of miR-598 could inhibit tumor cell metastasis in NSCLC. Conclusions: These findings for the first time revealed that miR-598, as a tumor suppressor, negatively regulate DERL1 and EMT to suppress the invasion and migration in NSCLC, thereby putatively serving as a novel therapeutic target for NSCLC clinical treatment.

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“…MicroRNAs (miRNAs) are non-coding RNAs found in multiple organisms, which can decrease levels of target mRNAs largely by binding to the 3'-untranslated regions (UTR) of target mRNAs (Bartel, 2004;Guo et al, 2010;Wu et al, 2006). MiRNAs proved to be potential biomarkers in many diseases in previous studies (Braga et al, 2017;Fkih M'hamed et al, 2017;Liu et al, 2017;Patoulias, 2018;Switlik et al, 2018). Among them, some studies have shown several miRNAs being abnormally expressed and may contribute to neuronal dysfunction (Hebert et al, 2008;Hebert and De Strooper, 2009).…”

Section: Introductionmentioning

confidence: 99%

MiR-361-3p inhibits β-amyloid accumulation and attenuates cognitive deficits through targeting BACE1 in Alzheimer's disease

Wang

Zhang

et al. 2019

Journal of Integrative Neuroscience

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The role of miR-361-3p in the pathology of Alzheimer's disease is unknown. The target scan was used to screen potential target genes of miR-361-3p, and β-site amyloid precursor protein (APP) cleaving enzyme 1 (BACE1) was emphasized. Results from western blotting and reverse transcription-quantitative polymerase chain reaction (RT-PCR) showed that down-regulated miR-361-3p was correlated with up-regulated BACE1 in Alzheimer's disease patients' brains. Luciferase assay confirmed that miR-361-3p directly targets BACE1. MiR-361-3p overexpression and knockdown experiments were performed and found that miR-361-3p could regulate the expression of BACE1, and the accumulation of APP-β in APPswe transfected SH-SY5Y cell. A Morris water maze test was performed and showed that overexpression of miR-361-3p improved cognitive deficits in APP/PS1 mice. We found miR-361-3p inhibited β-amyloid accumulation by targeting BACE1, which thus weakened cognitive deficits in Alzheimer's disease.

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MiR-598: A tumor suppressor with biomarker significance in osteosarcoma

Cited by 33 publications

References 31 publications

MicroRNA‑598 inhibits the proliferation and invasion of non‑small cell lung cancer cells by directly targeting ZEB2

MicroRNA‑598 inhibits the proliferation and invasion of non‑small cell lung cancer cells by directly targeting ZEB2

MiR-598 Suppresses Invasion and Migration by Negative Regulation of Derlin-1 and Epithelial-Mesenchymal Transition in Non-Small Cell Lung Cancer

MiR-361-3p inhibits β-amyloid accumulation and attenuates cognitive deficits through targeting BACE1 in Alzheimer's disease

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