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Altern Ther Health Med ; 29(8): 704-709, 2023 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-37708538

RESUMO

Objective: Abundant angiogenesis in hepatocellular carcinoma (HCC) is critical in its malignant course; however, its mechanism is incompletely understood. Meanwhile, the corresponding roles of PIK3R6 molecules in HCC have not been investigated. This study aims to explore the intrinsic mechanism of PIK3R6 and provide theoretical reference for the treatment of hepatocellular carcinoma. Methods: Differential expressions of PIK in ovarian cancer and normal ones were detected by Western blotting and quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Analyze the relationship between the expression of PIK3R6 and patient prognosis through the TCGA database. Subsequently constructed corresponding stable cell lines, combined with transcriptome sequencing and several cell biology experiments, we explored the inner mechanism and clinical significance of PIK3R6. Results: By analyzing multiple cohorts, we found that high PIK3R6 expression in tumor tissues negatively correlates with patient prognosis. PIK3R6 could increase angiogenesis in HCC by boosting the activity of the STAT3 signalling pathway to hasten the malignant progression of the disease, according to corresponding cellular and molecular experimental studies. Then again, immunohistochemistry on a series of tissue chips confirmed the important clinical significance of PIK3R6-STAT3 regulatory axis. Couclusions: This study initially addressed the clinical significance of PIK3R6 and revealed its mechanism for promoting angiogenesis in hepatocellular carcinoma, providing a reliable working foundation for future in-depth research and clinical translation.


Assuntos
Carcinoma Hepatocelular , Neoplasias Hepáticas , Humanos , Carcinoma Hepatocelular/genética , Carcinoma Hepatocelular/patologia , Neoplasias Hepáticas/genética , Neoplasias Hepáticas/patologia , Linhagem Celular Tumoral , Proliferação de Células , Transdução de Sinais , Fator de Transcrição STAT3/genética , Fator de Transcrição STAT3/metabolismo
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