Screening of key miRNAs and evaluation of their diagnostic and prognostic values in nasopharyngeal carcinoma

Zhuo, Xianlu; Zhou, Wei; Ye, Huiping; Li, Dairong; Chang, Aoshuang; Wu, Yongzhong; Zhou, Qi

doi:10.3892/ol.2019.10231

Cited by 6 publications

(3 citation statements)

References 27 publications

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“…Narrowly, an existed study has pronounced that upregulated miR-18a promotes NPC cell progression via mediation of DICER1 [6]. In addition, it is noticed that overexpressed miR-18a in NPC is believed to connect with NPC metastasis and repressed miR-18a partially contributes to better prognosis of NPC patients [31]. Lately, it is surveyed that downregulation of miR-18a is capable of discouraging NPC proliferation, invasion, and migration [4].…”

Section: Discussionmentioning

confidence: 99%

microRNA-18a from M2 Macrophages Inhibits TGFBR3 to Promote Nasopharyngeal Carcinoma Progression and Tumor Growth via TGF-β Signaling Pathway

Peng

Liu

et al. 2020

Nanoscale Res Lett

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Objectives Nasopharyngeal carcinoma (NPC) is a type of nasopharyngeal disease with high metastasis and invasion properties. Tumor-associated alternative activated (M2) macrophages are evidenced to connect with NPC. Based on this, this study purposes to explore the mechanism and participation of microRNA-18a (miR-18a) from M2 macrophages in NPC. Methods Peripheral blood mononuclear cells were differentiated to macrophages and macrophages were polarized to M2 type by interleukin-4. SUNE-1 and CNE2 cells were transfected with restored or depleted miR-18a or transforming growth factor-beta III receptor (TGFBR3) to explore their roles in NPC progression with the involvement of the TGF-β signaling pathway. Next, SUNE-1 and CNE2 cells were co-cultured with M2 macrophages that had been treated with restored or depleted miR-18a or TGFBR3 to comprehend their combined roles in NPC with the involvement of the TGF-β signaling pathway. Results MiR-18a was highly expressed and TGFBR3 was lowly expressed in NPC cells. MiR-18a restoration, TGFBR3 knockdown or co-culture with miR-18a mimics, or si-TGFBR3-transfected M2 macrophages promoted SUNE-1 cell progression, tumor growth in mice, decreased p-Smad1/t-Smad1, and elevated p-Smad3/t-Smad3. miR-18a downregulation, TGFBR3 overexpression, or co-culture with miR-18a inhibitors or OE-TGFBR3-transfected M2 macrophages depressed CNE2 cell progression, tumor growth in mice, increased p-Smad1/t-Smad1, and decreased p-Smad3/t-Smad3. Conclusion Our study elucidates that miR-18a from M2 macrophages results in promoted NPC cell progression and tumor growth in nude mice via TGFBR3 repression, along with the Smad1 inactivation and Smad3 activation.

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Section: Discussionmentioning

confidence: 99%

microRNA-18a from M2 Macrophages Inhibits TGFBR3 to Promote Nasopharyngeal Carcinoma Progression and Tumor Growth via TGF-β Signaling Pathway

Peng

Liu

et al. 2020

Nanoscale Res Lett

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“…It has been shown that as a member of the miR-17-92 cluster, the occurrence and development of tumors are tightly correlated with miR-18a. MiR-18a is related to tumor metastasis in nasopharyngeal carcinoma [24], astroglioma [25], breast cancer [26] and other tumor cells. The role of miR-18a in the pathogenesis of disease remains a challenging topic.…”

Section: Discussionmentioning

confidence: 99%

MiR-18a affects hypoxia induced glucose metabolism transition in HT22 hippocampal neuronal cell line through the Hif1a gene

Liu,

Zuo

et al. 2024

BMC Neurol

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Hypoxia can cause a variety of diseases, including ischemic stroke and neurodegenerative diseases. Within a certain range of partial pressure of oxygen, cells can respond to changes in oxygen. Changes in oxygen concentration beyond a threshold will cause damage or even necrosis of tissues and organs, especially for the central nervous system. Therefore, it is very important to find appropriate measures to alleviate damage. MiRNAs can participate in the regulation of hypoxic responses in various types of cells. MiRNAs are involved in regulating hypoxic responses in many types of tissues by activating the hypoxia-inducible factor (HIF) to affect angiogenesis, glycolysis and other biological processes. By analyzing differentially expressed miRNAs in hypoxia and hypoxia-related studies, as well as the HT22 neuronal cell line under hypoxic stress, we found that the expression of miR-18a was changed in these models. MiR-18a could regulate glucose metabolism in HT22 cells under hypoxic stress by directly regulating the 3’UTR of the Hif1a gene. As a small molecule, miRNAs are easy to be designed into small nucleic acid drugs, so this study can provide a theoretical basis for the research and treatment of nervous system diseases caused by hypoxia. Graphical Abstract

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“…The incidence rate of NPC is high in Asia [16]. RT for various malignant tumors is an effective, standard therapeutic intervention that is commonly used.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of miR-140-3p Could Reverse Radioresistance of Nasopharyngeal Carcinoma by Targeting XIAP

Zhu

2020

Preprint

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BackgroundMalignant behavior and radioresistance, which severely limits the efficacy of radiotherapy (RT) in nasopharyngeal carcinoma (NPC), lead to tumor progression and poor prognosis. The aim of this study was to investigate the underlying molecular mechanism of miR-140-3p on NPC development and radioresistance.MethodsThe expression of genes and proteins was detected by Western blotting, and quantitative reverse transcription PCR (qRT-PCR). Proliferation, apoptosis, and radioresistance of NPC were detected. Luciferase reporter assays were used to detect the interactions of miR-140-3p with its downstream targets.ResultsThe expression of miR-140-3p was associated with the occurrence and radiation resistance of NPC. XIAP as the direct target of miR-140-3p was verified. We found alleviated radioresistance of NPC cells upon miR-140-3p overexpression or XIAP knockdown.ConclusionmiR-140-3p is downregulated in radioresistant NPC. miR-140-3p could hamber radioresistance of NPC via directly target XIAP, suggesting miR-140-3p/XIAP axis is vital in the regulation of irradiation sensitivity.

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Screening of key miRNAs and evaluation of their diagnostic and prognostic values in nasopharyngeal carcinoma

Cited by 6 publications

References 27 publications

microRNA-18a from M2 Macrophages Inhibits TGFBR3 to Promote Nasopharyngeal Carcinoma Progression and Tumor Growth via TGF-β Signaling Pathway

microRNA-18a from M2 Macrophages Inhibits TGFBR3 to Promote Nasopharyngeal Carcinoma Progression and Tumor Growth via TGF-β Signaling Pathway

MiR-18a affects hypoxia induced glucose metabolism transition in HT22 hippocampal neuronal cell line through the Hif1a gene

Overexpression of miR-140-3p Could Reverse Radioresistance of Nasopharyngeal Carcinoma by Targeting XIAP

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Screening of key miRNAs and evaluation of their diagnostic and prognostic values in nasopharyngeal carcinoma

Cited by 6 publications

References 27 publications

microRNA-18a from M2 Macrophages Inhibits TGFBR3 to Promote Nasopharyngeal Carcinoma Progression and Tumor Growth via TGF-β Signaling Pathway

microRNA-18a from M2 Macrophages Inhibits TGFBR3 to Promote Nasopharyngeal Carcinoma Progression and Tumor Growth via TGF-β Signaling Pathway

MiR-18a affects hypoxia induced glucose metabolism transition in HT22 hippocampal neuronal cell line through the Hif1a gene

Overexpression of miR-140-3p&nbsp;Could Reverse Radioresistance of Nasopharyngeal Carcinoma by Targeting XIAP

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Overexpression of miR-140-3p Could Reverse Radioresistance of Nasopharyngeal Carcinoma by Targeting XIAP