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1.
Biomedical and Environmental Sciences ; (12): 241-252, 2023.
Artículo en Inglés | WPRIM | ID: wpr-970313

RESUMEN

OBJECTIVE@#Programmed cell death 6 (PDCD6), a Ca 2+-binding protein, has been reported to be aberrantly expressed in all kinds of tumors. The aim of this study was to explore the role and mechanism of PDCD6 in hepatocellular carcinomas (HCCs).@*METHODS@#The expression levels of PDCD6 in liver cancer patients and HCC cell lines were analyzed using bioinformatics and Western blotting. Cell viability and metastasis were determined by methylthiazol tetrazolium (MTT) and transwell assays, respectively. And Western blotting was used to test related biomarkers and molecular pathway factors in HCC cell lines. LY294002, a PI3K inhibitor inhibiting AKT, was used to suppress the AKT/GSK3β/β-catenin pathway to help evaluate the role of this pathway in the HCC carcinogenesis associated with PDCD6.@*RESULTS@#The analysis of The Cancer Genome Atlas Database suggested that high PDCD6 expression levels were relevant to liver cancer progression. This was consistent with our finding of higher levels of PDCD6 expression in HCC cell lines than in normal hepatocyte cell lines. The results of MTT, transwell migration, and Western blotting assays revealed that overexpression of PDCD6 positively regulated HCC cell proliferation, migration, and invasion. Conversely, the upregulation of PDCD6 expression in the presence of an AKT inhibitor inhibited HCC cell proliferation, migration, and invasion. In addition, PDCD6 promoted HCC cell migration and invasion by epithelial-mesenchymal transition. The mechanistic investigation proved that PDCD6 acted as a tumor promoter in HCC through the AKT/GSK3β/β-catenin pathway, increasing the expression of transcription factors and cellular proliferation and metastasis.@*CONCLUSION@#PDCD6 has a tumor stimulative role in HCC mediated by AKT/GSK3β/β-catenin signaling and might be a potential target for HCC progression.


Asunto(s)
Humanos , Carcinoma Hepatocelular/patología , Neoplasias Hepáticas/patología , Proteínas Proto-Oncogénicas c-akt/metabolismo , beta Catenina/metabolismo , Fosfatidilinositol 3-Quinasas/metabolismo , Glucógeno Sintasa Quinasa 3 beta/metabolismo , Línea Celular , Proliferación Celular , Línea Celular Tumoral , Regulación Neoplásica de la Expresión Génica , Proteínas de Unión al Calcio/metabolismo , Proteínas Reguladoras de la Apoptosis/genética
2.
International Eye Science ; (12): 1391-1393, 2014.
Artículo en Chino | WPRIM | ID: wpr-641967

RESUMEN

AIM: To study the expressions and clinical significance of PDCD4 and B7-H4 in optic gliomas in children. METHODS:We used immunohistochemistry to evaluate the expressions of PDCD4 and B7-H4 in specimens from 52 optic gliomas in children cases, and analyzed the correlation of PDCD4 and B7 - H4 expression with clinicopathological factors children optic gliomas. RESULTS: PDCD4 expression reduced in optic glioma tissue:PDCD4 expression rate in 52 cases of optic glioma tissues decreasing was correlated with tumor malignancy increase (P CONCLUSION: Expressions of PDCD4 and B7-H4 may be clinically relevant to tumor malignancy of optic gliomas in children and prevention of metastasis and prediction of prognosis.

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