miR-454-3p exerts tumor-suppressive functions by down-regulation of NFATc2 in glioblastoma

Zuo, Jiandong; Yu, Huimei; Xie, Peng; Liu, Wenguang; Wang, Kai; Ni, Hongzao

doi:10.1016/j.gene.2019.06.008

Cited by 30 publications

(25 citation statements)

References 20 publications

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“…For instance, miR-6852 expression is downregulated in glioma and suppresses cell proliferation, migration and invasion by targeting lymphoid enhancer-binding factor 1 (38). miR-454-3p exerts tumor-suppressive functions in glioblastoma, inhibiting cell proliferation and inducing apoptosis by targeting nuclear factor of activated T-cells, cytoplasmic 2 (39). Several studies have reported that miR-mediates disease progression in various types of cancer.…”

Section: Multivariate Analysis --------------------------------------mentioning

confidence: 99%

miR‑665 is downregulated in glioma and inhibits tumor cell proliferation, migration and invasion by targeting high mobility group box 1

Shen

You

et al. 2020

Oncol Lett

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Section: Multivariate Analysis --------------------------------------mentioning

confidence: 99%

miR‑665 is downregulated in glioma and inhibits tumor cell proliferation, migration and invasion by targeting high mobility group box 1

Shen

You

et al. 2020

Oncol Lett

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“…It was observed by Bao et al that as a histone methyltransferase, EZH2 could be recruited in the miR-454-3p promoter to induce miR-454-3p DNA methylation and thus decrease miR-454-3p expression in chondrosarcoma cells (Bao et al, 2017), which was coincident with our results that EZH2 inhibited miR-454-3p by DNA methylation. Additionally, results from a recent study unraveled that miR-454-3p downregulation was observed in glioblastoma cells and tissues and its downregulation could promote cell proliferation and repress cell apoptosis (Zuo et al, 2019). This study demonstrated that inhibition of miR-454-3p in glioma cells promoted M2 macrophage polarization, corresponding to elevated expression of II1b, Cd86, and Nos2, and reduced expression of Cd163, Ym1 and Mrc1 in macrophages.…”

Section: Discussionmentioning

confidence: 62%

EZH2-Inhibited MicroRNA-454-3p Promotes M2 Macrophage Polarization in Glioma

Yang

Zhu

et al. 2020

Front. Cell Dev. Biol.

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Glioma is a primary intracranial tumor with high incidence and mortality. The oncogenic role of EZH2 has been reported in glioma. EZH2 inhibited microRNA-454-3p (miR-454-3p) by binding to its promoter in chondrosarcoma cells. Therefore, our study aimed to identify whether EZH2 regulated M2 macrophage polarization in glioma via miR-454-3p. Clinical samples of different grades of glioma and glioma cells were collected and immunohistochemistry and RT-qPCR demonstrated that EZH2 was highly expressed in glioma tissues. Expression of EZH2 was positively correlated with the degree of M2 macrophage polarization in glioma tissues. EZH2 was silenced by lentivirus in glioma cells, which were subsequently co-cultured with macrophages to evaluate its effect on macrophage polarization. miR-454-3p, a down-regulated miR in glioma, was found to be increased after silencing of EZH2. Furthermore, MethPrimer analysis showed that EZH2 silencing inhibited the DNA methylation level of miR-454-3p. Additionally, MS-PCR, dual-luciferase reporter, RIP and RNA pull down assays revealed that miR-454-3p promoted PTEN expression by inhibiting m6A modification through binding to the enzyme YTHDF2. Either inhibition of miR-454-3p or PTEN resulted in promotion of M2 macrophage polarization. Collectively, histone methyltransferase EZH2 inhibited miR-454-3p through methylation modification and promoted m6A modification of PTEN to induce glioma M2 macrophage polarization.

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“…miR-454-3p promoted breast cancer metastasis by suppressing the regulation of nuclear pre-mRNA domain containing 1A and by activating Wingless/Integrated signaling (26). Furthermore, miR-454-3p may act as a tumor suppressor; a previous study demonstrated miR-454-3p downregulation in glioblastoma and that it exerted tumor-suppressive functions by targeting nuclear factor of activated T cells, cytoplasmic 1 (17). By inhibiting signal transducer and activator of transcription 3 and autophagy-related protein 12, miR-454-3p negatively regulated the growth of chondrosarcoma (16).…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, in the present study, ox-LDL-induced HAECs were used as atherosclerosis cell models to explore the molecular mechanism underlying atherosclerosis. Although the role of miR-454-3p in tumorigenesis is well documented (14)(15)(16)(17), its involvement in the regulation of HAEC apoptosis remains to be elucidated. The present study investigated the role of miR-454-3p in cell apoptosis in atherosclerosis.…”

Section: Introductionmentioning

confidence: 99%

miR‑454‑3p prevents ox‑LDL‑induced apoptosis in HAECs by targeting TRPC3

Liao

Yang

et al. 2021

Exp Ther Med

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Endothelial-cell (EC) apoptosis serves a vital role in the pathogenesis of atherosclerosis. Accumulating evidence has implicated microRNA (miRNA/miR) dysregulation in EC apoptosis. Although the role of miR-454-3p in carcinogenesis has been well documented, its role and underlying mechanism in EC apoptosis remain unclear. In the present study, the results revealed that miR-454-3p expression was substantially downregulated in human aortic endothelial cells (HAECs) following oxidized low-density lipoprotein (ox-LDL) treatment. miR-454-3p suppression significantly attenuated the viability of HAECs, while miR-454-3p overexpression repressed ox-LDL-induced HAEC apoptosis. Bioinformatics analysis and luciferase reporter assays revealed that transient receptor potential canonical 3 (TRPC3), a key regulator of atherosclerosis development, was the direct target of miR-454-3p. Furthermore, TRPC3 overexpression abolished the anti-apoptotic effect of miR-454-3p on HAECs. These results revealed a novel role of miR-454-3p in ox-LDL-induced apoptosis in HAECs.

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miR-454-3p exerts tumor-suppressive functions by down-regulation of NFATc2 in glioblastoma

Cited by 30 publications

References 20 publications

miR‑665 is downregulated in glioma and inhibits tumor cell proliferation, migration and invasion by targeting high mobility group box 1

miR‑665 is downregulated in glioma and inhibits tumor cell proliferation, migration and invasion by targeting high mobility group box 1

EZH2-Inhibited MicroRNA-454-3p Promotes M2 Macrophage Polarization in Glioma

miR‑454‑3p prevents ox‑LDL‑induced apoptosis in HAECs by targeting TRPC3

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