1,833,239 research outputs found
vIRF1 suppresses miR-218-5p via hypermethylation of the pre-miR-218-1 promoter.
No full text(A). qPCR showing SLIT2 and SLIT3 expression in vIRF1-transduced HUVECs. (B). qPCR showing SLIT2 and SLIT3 expression in KSHV-infected HUVECs. (C). qPCR showing pre-miR-218-1 expression in vIRF1-transduced HUVECs. (D). qPCR showing pre-miR-218-1 expression in KSHV-infected HUVECs (E). Methylation-specific PCR showing DNA methylation of in the pre-miR-218-1 promoter in vIRF1-transduced HUVECs. (F). Methylation-specific PCR showing DNA methylation of the pre-miR-218-1 promoter in KSHV-infected cells. (G). qPCR showing miR-218-5p expression in vIRF1-transduced HUVECs treated with 5-aza. (H). Western-blotting of HMGB2 and CMPK1 expression in vIRF1-transduced HUVECs treated with 5-aza. The Western blots were ran with the same samples but in two different gels, with each of them calibrated by independent GAPDH panels. The quantified results represent mean ± SD. *** P < 0.001, Student's t-test. undet., undetermined.</p
miR-218-5p directly targets HMGB2 and CMPK1 3'UTR.
No full text(A). Luciferase activity in HEK293T cells cotransfected with miR-218-5p mimic (miR-218-5p; 10 nM) or its control (NC of mimic; 10 nM) and the reporter constructs for 48 h. (B). Luciferase activity in HEK293T cells cotransfected with increasing amounts of miR-218-5p mimic (miR-218-5p; 5, 10, and 15 nM) or its control (NC of mimic), and the pGL-3-HMGB2 3'UTR reporter or pGL-3-CMPK1 3'UTR reporter for 48 h. (C). Western blotting of HMGB2 and CMPK1 expression in HUVECs transfected with increasing amounts of miR-218-5p mimic (10, 20 and 40 nM) or its control for 48 h. (D). Western blotting of HMGB2 and CMPK1 expression in HUVECs transfected with a miR-218-5p inhibitor for 48 h. (E). Putative binding site of miR-218-5p in the 3'UTR region of HMGB2 and mutagenesis of target site in miR-218-5p. (F). Putative binding site of miR-218-5p in the 3'UTR region of CMPK1 and mutagenesis of target site in miR-218-5p. (G). Luciferase activity in HEK293T cells cotransfected with miR-218-5p mimic (miR-218-5p; 10 nM), miR-218-5p mutant mimic (miR-218-5p mut 1; 10 nM) or a negative control (NC of mimic; 10 nM), and the HMGB2 3'UTR or CMPK1 3'UTR reporter construct for 48 h. (H). Western-blotting of HMGB2 and CMPK1 expression in HUVECs transfected with a negative control mimic (NC of mimic; 20 nM), miR-218-5p mimic (miR-218-5p mimic; 20 nM) or miR-218-5p mutant mimic (miR-218-5p mut 1; 20 nM) for 48 h, respectively. The quantified results represent mean ± SD. Results are from three independent experiments, each with quadruple technical replicates, were performed. * P P P ### P n.s, not significant.</p
C-218 INICIA CICLO DE CONFERENCIAS SOBRE LAS CIENCIAS MÉDICO BIOLÓGICAS RUMBO AL ESPACIO
No full textC-218 INICIA CICLO DE CONFERENCIAS SOBRE LAS CIENCIAS MÉDICO BIOLÓGICAS RUMBO AL ESPACIOC-218 INICIA CICLO DE CONFERENCIAS SOBRE LAS CIENCIAS MÉDICO BIOLÓGICAS RUMBO AL ESPACIODO
C-218 INICIA CICLO DE CONFERENCIAS SOBRE LAS CIENCIAS MÉDICO BIOLÓGICAS RUMBO AL ESPACIO
No full textC-218 INICIA CICLO DE CONFERENCIAS SOBRE LAS CIENCIAS MÉDICO BIOLÓGICAS RUMBO AL ESPACIOC-218 INICIA CICLO DE CONFERENCIAS SOBRE LAS CIENCIAS MÉDICO BIOLÓGICAS RUMBO AL ESPACIOPD
vIRF1 suppresses miR-218-5p via hypermethylation of the pre-miR-218-1 promoter by inhibiting p53 to increase DNMT1 expression.
No full text(A). Western-blotting of DNMT1 expression in vIRF1-transduced HUVECs. (B). Western-blotting of DNMT1 in KSHV-infected HUVECs. (C). Methylation-specific PCR showing DNA methylation of the pre-miR-218-1 promoter in vIRF1-expressing HUVECs transfected with a mixture of siRNAs targeting DNMT1 (siDNMT1). (D). qPCR showing DNMT1, SLIT2, pre-miR-218-1 and miR-218-5p expression in vIRF1-expressing HUVECs transfected with a mixture of siRNAs targeting DNMT1 (siDNMT1). (E). Western-blotting of DNMT1, HMGB2 and CMPK1 expression in vIRF1-expressing HUVECs transfected with a mixture of siRNAs targeting DNMT1 (siDNMT1). (F). Western-blotting of DNMT1, HMGB2 and CMPK1 expression in vIRF1-expressing HUVECs transfected with pCMV6-Entry-C-Myc-p53 construct. The Western blots were ran with the same samples but in two different gels, with each of them calibrated by independent GAPDH panels. (G). Methylation-specific PCR showing DNA methylation of the pre-miR-218-1 promoter in vIRF1-expressing HUVECs transfected with pCMV6-Entry-C-Myc-p53 construct. (H). qPCR showing pre-miR-218-1 and miR-218-5p expression in vIRF1-expressing HUVECs transfected with pCMV6-Entry-C-Myc-p53 construct. The quantified results represent mean ± SD. * P P P < 0.001, Student's t-test.</p
C-218 INICIA CICLO DE CONFERENCIAS SOBRE LAS CIENCIAS MÉDICO BIOLÓGICAS RUMBO AL ESPACIO
No full textC-218 INICIA CICLO DE CONFERENCIAS SOBRE LAS CIENCIAS MÉDICO BIOLÓGICAS RUMBO AL ESPACI
C-218 INICIA CICLO DE CONFERENCIAS SOBRE LAS CIENCIAS MÉDICO BIOLÓGICAS RUMBO AL ESPACIO
No full textC-218 INICIA CICLO DE CONFERENCIAS SOBRE LAS CIENCIAS MÉDICO BIOLÓGICAS RUMBO AL ESPACI
LIPIcs, Volume 218, FORC 2022, Complete Volume
No full textLIPIcs, Volume 218, FORC 2022, Complete Volum
MicroRNA-218-5p affects lung adenocarcinoma progression through targeting endoplasmic reticulum oxidoreductase 1 alpha
No full textLung adenocarcinoma (LUAD) severely threatens the health of people owing to its lethality. Nonetheless, the underlying mechanisms on LUAD development remain unclear to a great extent. This work aimed to probe the functions of miR-218-5p in LUAD. MiR-218-5p and endoplasmic reticulum oxidoreductase 1 alpha (ERO1A) were screened as differently downregulated and upregulated RNAs in LUAD, respectively, by bioinformatics analyses. The results of cell functional assays stated that enforced expression of miR-218-5p notably restrained cell viability, invasion, and migration in LUAD. MiR-218-5p may interact with 3’-untranslated region of ERO1A mRNA as analyzed by bioinformatics. Afterward, western blot and dual-luciferase reporter gene analyses were introduced to identify their interaction. ERO1A overexpression reversed the suppressive impacts of miR-218-5p on LUAD cell progression, indicating the implication of miR-218-5p/ERO1A axis in suppressing cancer development. We also observed that this regulatory axis suppressed angiogenesis in LUAD. Taken together, miR-218-5p/ERO1A axis exerted an imperative role in LUAD cell progression, which provides a valuable clue for the development of LUAD therapeutic regimen.</p
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