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1.
Cancer Sci ; 2019 Nov 28.
Artigo em Inglês | MEDLINE | ID: mdl-31778279

RESUMO

Metastasis is a critical determinant for the treatment strategy and prognosis in patients with squamous cell carcinoma of the head and neck (SCCHN). However, the mechanisms underlying SCCHN metastasis are poorly understood. Our study sought to determine the key microRNA and their functional mechanisms involved in SCCHN metastasis. For The Cancer Genome Atlas (TCGA) data analysis, quantitative PCR was used to quantify the level of miR-30e-5p in SCCHN and its clinical significance was further analyzed. A series of in vitro and in vivo experiments were applied to determine the effects of miR-30e-5p and its target AEG-1 on SCCHN metastasis. A mechanism investigation further revealed that AEG-1 was implicated in the angiogenesis and metastasis mediated by miR-30e-5p. Overall, our study confirms that miR-30e-5p is a valuable predictive biomarker and potential therapeutic target in SCCHN metastasis.

2.
Biol Reprod ; 101(4): 664-674, 2019 Oct 25.
Artigo em Inglês | MEDLINE | ID: mdl-31291448

RESUMO

Evidence indicates that microRNAs (miRNAs) play essential roles in early embryonic development. The miRNA-518 family is a special biomarker of the placenta, and miRNA-518b is abnormally expressed in placental tissue in preeclampsia. Early growth response protein 1 (EGR1), a zinc finger transcriptional factor, plays an essential role in regulating cell differentiation, angiogenesis, and migration. Moreover, earlier studies have shown that EGR1 protein plays a key role in implantation. However, little is known about the role of miR-518b and EGR1 on early embryonic arrest (EEA) in humans. In our study, increased miR-518b along with decreased EGR1 was found in human villus tissues with EEA. Furthermore, we demonstrated by luciferase assay that miR-518b is a direct regulator of EGR1. After comparing the effect of silencing EGR1, vascular endothelial growth factor (VEGF) individually, and EGR1/VEGF in combination, we found that EGR1 can inhibit migration and angiogenesis of HTR-8 SVneo cells by decreasing the VEGF expression. Hypoxia plays an initial role in early embryonic development, and we found that hypoxia reduces the expression of miR-518b and increases the expression of EGR1 and VEGF to facilitate migration and angiogenesis in a hypoxic model of HTR-8/SVneo cell line. Our findings provide new insights into the role of miR-518b in EEA and implicate the potential application of miR-518b in the diagnosis and development of intervention for EEA.

3.
Gene ; 697: 19-25, 2019 May 20.
Artigo em Inglês | MEDLINE | ID: mdl-30776465

RESUMO

Early Embryonic Arrest (EEA) is one of the major causes of female infertility. Genetic factors including specific genes and miRNAs may play pivotal roles on EEA. However, it is not well defined what genes and micro RNAs participate the pathophysiological alterations of EEA. In this work, we compared the Transcriptome -Seq and microRNA profiles from three pairs of villi (three EEA patients and three normal pregnancy, NP). We first confirmed the array data by qPCR with ten randomly selected differentially expressed genes and ten differentially expressed miRNAs in villi from 20 EEA and 20 NP controls. We next applied Gene ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) Pathway analysis and found that these differentially expressed genes enriched in the PI3K-Akt signaling pathway, Jak-STAT signaling pathway, MAPK signaling pathway, Complement and coagulation cascades, Hypertrophic cardiomyopathy (HCM), Dilated cardiomyopathy (DCM). Interestingly, hsa-miR-6515-5p and its target genes NLRP3, UGP2 may regulate the Immune system and carbohydrate metabolism. Hsa-miRNA 518 and its target gene EGR1 may regulate cell proliferation, angiogenesis, and cell apoptosis to impact early embryonic development. Moreover, novel-m0045-5p and its target gene RMDN3 may regulate microtubule formation on the development of EEA. Our research provides novel biomarkers for EEA and establishes a foundation for further study of the mechanism of EEA.


Assuntos
Perda do Embrião/genética , Desenvolvimento Embrionário/genética , MicroRNAs/genética , Adulto , Grupo com Ancestrais do Continente Asiático/genética , Vilosidades Coriônicas/fisiologia , Feminino , Perfilação da Expressão Gênica , Sequenciamento de Nucleotídeos em Larga Escala/métodos , Humanos , Infertilidade Feminina/genética , Gravidez , Transdução de Sinais , Transcriptoma , Sequenciamento Completo do Exoma/métodos
4.
PLoS One ; 13(8): e0202883, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30142203

RESUMO

During the atmospheric correction of remote sensing data in inland waters, the original Second Simulation of the Satellite Signal in the Solar Spectrum-Vector version (6SV) model does not eliminate the specular reflection of downward skylight radiance at the air-water interface. Thus, we propose a modified version of the 6SV model (M6SV) that does remove reflected skylight at the air-water interface. We apply the new model to the atmospheric correction of a Landsat 8 Operational Land Imager (OLI) image over Taihu Lake, China, where the aerosol optical depth is known. In situ reflectance measurements acquired concurrently with the L8/OLI image are used to validate the performance of the new M6SV algorithm. To further analyze the merits and demerits of M6SV, the model is compared with two short-wave infrared (SWIR)-based atmospheric correction models: the Sea-Viewing Wide Field-of-View Sensor Data Analysis System short-wave infrared (SD-SWIR) model and the Vanhellemont & Ruddick short-wave infrared with a per scene fixed aerosol type (VR-SWIR-F) model. Comparisons of results from all three L8/OLI image atmospheric corrections with the in situ remote sensing reflectance data show that M6SV produces reliable atmospheric corrections in the green and red spectral bands and is an effective alternative for Landsat 8 OLI atmospheric correction in inland waters.


Assuntos
Ar , Processamento de Imagem Assistida por Computador , Modelos Teóricos , Imagens de Satélites , Água , Algoritmos
5.
Gene ; 652: 48-58, 2018 Apr 30.
Artigo em Inglês | MEDLINE | ID: mdl-29427737

RESUMO

Nasopharyngeal carcinoma (NPC) is a head and neck cancer associated with poor prognosis. Many studies have shown that the epithelial-to-mesenchymal transition (EMT) is important in cancer progression, metastasis, and chemotherapy resistance and that microRNAs (miRNAs) play a key role in chemotherapy resistance associated with EMT. The miRNA miR-139-5p is downregulated in many human cancers and is closely related to tumor progression. The aim of this study was to investigate the ability of miR-139-5p to influence the cisplatin resistance, apoptosis, invasion and migration in NPC cells through the regulation of the EMT. We investigated these processes in parental HNE1 and cisplatin-resistant HNE1/DDP cells transfected with miR-139-5p inhibitors and mimics, respectively. Our results suggest that the upregulation of miR-139-5p expression inhibits proliferation, invasion, migration and EMT in human NPC cells. In addition, we found that miR-139-5p expression levels and DDP-induced apoptosis positively correlate in NPC cells. In conclusion, our results demonstrate that miR-139-5p can regulate the migration, invasion and DDP resistance in human NPC by modulating the EMT. The regulation of miR-139-5p levels might be a new approach to reverse EMT and DDP resistance and counteract metastasis and chemotherapy resistance in human NPC.


Assuntos
Antineoplásicos/farmacologia , Cisplatino/farmacologia , Células Epiteliais/efeitos dos fármacos , Transição Epitelial-Mesenquimal/efeitos dos fármacos , Regulação Neoplásica da Expressão Gênica , MicroRNAs/genética , Linhagem Celular Tumoral , Movimento Celular , Resistencia a Medicamentos Antineoplásicos/genética , Células Epiteliais/metabolismo , Células Epiteliais/patologia , Transição Epitelial-Mesenquimal/genética , Humanos , MicroRNAs/antagonistas & inibidores , MicroRNAs/metabolismo , Mimetismo Molecular , Nasofaringe/efeitos dos fármacos , Nasofaringe/metabolismo , Nasofaringe/patologia , Oligorribonucleotídeos Antissenso/genética , Oligorribonucleotídeos Antissenso/metabolismo
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