Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 3 de 3
Filtrar
Mais filtros










Filtros aplicados
Base de dados
Intervalo de ano de publicação
1.
Clin. transl. oncol. (Print) ; 26(1): 119-135, jan. 2024.
Artigo em Inglês | IBECS | ID: ibc-229151

RESUMO

Background Protein phosphatase 1 regulatory subunit 14B (PPP1R14B) is an oncogenic gene found in a variety of tumors, but its role in the prognosis and development of kidney renal clear cell carcinoma (KIRC) remains unknown. Our study aimed to determine whether PPP1R14B could be a prognostic biomarker for KIRC and its role in the development of KIRC. Methods In this work, we used The Cancer Genome Atlas (TCGA) database to explore the expression of PPP1R14B in tumor tissues, its relationship with the prognosis of tumor patients, and its role in tumor occurrence and development. We validated our findings using the International Cancer Genome Consortium (ICGC) cohort, our clinical samples, and in vitro experiments. Results PPP1R14B was upregulated in KIRC compared to adjacent normal tissue. Moreover, multivariate analysis revealed that upregulated PPP1R14B expression was an independent risk factor for KIRC progression. High-PPP1R14B groups had shorter overall survival (OS) and disease-free survival (DFS) in TCGA and ICGC cohorts. We used Cell Counting Kit-8 (CCK8) and scratch wound healing assay to explore the proliferation and migration of KIRC cells following PPP1R14B knockdown. Our results indicated that PPP1R14B knockdown significantly reduced the proliferation and migration of KIRC cells in vitro. We also explored the possible cellular mechanisms of PPP1R14B through the Kyoto Encyclopedia of Genes and Genomes (KEGG), Gene ontology (GO) analysis, and TISIDB analysis. The function enrich analysis revealed that PPP1R14B-related genes were mainly enriched in purine metabolism and the macromolecule catabolic process. PPP1R14B expression was associated with tumor-infiltrating immune cells (TIICs) in the TCGA cohort, and the results of single-cell RNA-seq (scRNA) further demonstrated that PPP1R14B expression was associated with the enhanced infiltration of CD8 + T lymphocytes (AU)


Assuntos
Humanos , Biomarcadores Tumorais/sangue , Carcinoma de Células Renais/sangue , Carcinoma de Células Renais/genética , Neoplasias Renais/genética , Proteína Fosfatase 1/sangue , Prognóstico
2.
Clin. transl. oncol. (Print) ; 24(6): 1115-1123, junio 2022.
Artigo em Inglês | IBECS | ID: ibc-203810

RESUMO

PurposeIn the present work, we investigated the expression pattern of miR-4463 in the non-metastasis and metastasis colorectal cancer (CRC) patients and its regulation axis.MethodsRT-qPCR assay was performed to assess miR-4463 expression in the serum and tissues of patients with non-metastasis and metastasis, and in the CRC cell lines. MTT assay, colony formation assay, transwell assay, and flow cytometry assay were used to examine the role of miR-4463 in CRC cell viability, proliferation, and migration. Bioinformatic analysis was used to identify the potential target gene of miR-4463, and the targeting relationship between miR-4463 and PPP1R12B was verified in vitro using dual luciferase assay. Western blotting assay was used to determine the protein level of the target gene PPP1R12B in CRC cells under the transfections of miR-4463 mimic, inhibitor and vectors overexpressing PPP1R12B.ResultsmiR-4463 was markedly increased in the non-metastasis CRC tissues, and increased even higher in the metastasis CRC tissues, while miR-4463 expression had no significant difference in serum from non-metastasis and metastasis CRC samples. Besides, miR-4463 was upregulated in CRC cell lines. Functionally, miR-4463 promoted CRC cell proliferation, migration, and inhibiting cell apoptosis. Further analysis revealed that the miR-4463/PPP1R12B axis was responsible for the role of this miRNA.ConclusionWe reported the roles of miR-4463 in CRC proliferation and migration, supporting that miR-4463 could be a potential predictive diagnostic marker for colon cancer.


Assuntos
Humanos , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células , Neoplasias do Colo/genética , Neoplasias do Colo/metabolismo , Neoplasias do Colo/patologia , MicroRNAs/genética , MicroRNAs/metabolismo , Proteína Fosfatase 1/biossíntese , Proteína Fosfatase 1/genética , Proteína Fosfatase 1/metabolismo
3.
J. physiol. biochem ; 63(3): 203-212, jul.-sept. 2007. ilus, graf
Artigo em Inglês | IBECS | ID: ibc-76677

RESUMO

The mechanisms involved in the neuroprotective effect of serotonin 5-HT1Areceptor agonists on brain damage induced by ischemia remain to be fully elucidated.Given that serotonergic drugs may regulate N-methyl-D-aspartate (NMDA)receptor function, which is implicated in events leading to ischemia-induced neuronalcell death, this study sought to determine the effects of the selective 5-HT1Areceptor agonist, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), on thelevels of NMDA receptor NR1 subunit in gerbil hippocampus after transient globalcerebral ischemia. Pretreatment with 8-OH-DPAT (1 mg/kg) prevented the neuronalloss in CA1 subfield 72 h after ischemia. NMDA receptor NR1 levels in wholehippocampus were not affected 24 h after ischemia, but the levels of the subunitphosphorylated at the protein kinase A (PKA) site, pNR1(Ser897), were significantlyincreased, and this increase was prevented by the same 8-OH-DPAT dose, a probableconsequence of the increased phosphatase 1 (PP1) enzyme activity found inischemic gerbils pretreated with the 5-HT1A receptor agonist. The results suggestthat NR1 subunit phosphorylation plays a role in the neuroprotective effect of 8-OH-DPAT on cell damage induced by global cerebral ischemia in the gerbil hippocampusand support the potential interest of 5-HT1A receptor activation in thesearch for neuroprotective strategies (AU)


No disponible


Assuntos
Animais , Masculino , 8-Hidroxi-2-(di-n-propilamino)tetralina/farmacologia , Ataque Isquêmico Transitório/fisiopatologia , Fármacos Neuroprotetores/farmacologia , Receptor 5-HT1A de Serotonina/metabolismo , Receptores de N-Metil-D-Aspartato/metabolismo , Gerbillinae , Hipocampo/metabolismo , Ataque Isquêmico Transitório/tratamento farmacológico , Fosforilação , Proteína Fosfatase 1/metabolismo
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...