UBE2L3 expression in human gastric cancer and its clinical significance.
J Cancer Res Clin Oncol
; 150(4): 210, 2024 Apr 24.
Article
en En
| MEDLINE
| ID: mdl-38656363
ABSTRACT
PURPOSE:
Gastric cancer (GC) is prevalent as one of the most common malignant tumors globally, with a particularly high incidence in China. The role of UBE2L3 in the initiation and progression of various cancers has been well documented, but its specific significance in GC is not yet fully elucidated. The objective of this study is to examine the expression and importance of UBE2L3 in human gastric cancer tissues.METHODS:
Immunohistochemical staining and survival analysis were conducted on 125 cases of GC. Western blot and quantitative real-time polymerase chain reaction (qRT-PCR) were employed to assess the expression of UBE2L3 in GC cell lines. Cell lines with UBE2L3 knockdown and overexpression were cultured through lentivirus transfection and subsequently assessed using Western blot analysis. The involvement of UBE2L3 in the proliferation, invasion, and apoptosis of GC cells was confirmed through in vitro experiments, and its capacity to facilitate tumor growth was also validated in in vivo studies.RESULTS:
The up-regulation of UBE2L3 expression was observed in GC, and its high expression was found to be significantly associated with the degree of differentiation (χ2 = 6.153, P = 0.0131), TNM stage (χ2 = 6.216, P = 0.0447), and poor overall survival. In vitro, UBE2L3 has been shown to enhance functions in GC cell lines, such as promoting proliferation and invasion, and inhibiting apoptosis. In vivo experiments have validated the role of UBE2L3 in promoting tumor growth.CONCLUSIONS:
The findings of our study demonstrate the significant involvement of UBE2L3 in the pathogenesis and advancement of gastric cancer, suggesting its potential as a therapeutic target.Palabras clave
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Base de datos:
MEDLINE
Asunto principal:
Neoplasias Gástricas
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Apoptosis
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Enzimas Ubiquitina-Conjugadoras
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Proliferación Celular
Idioma:
En
Revista:
J Cancer Res Clin Oncol
Año:
2024
Tipo del documento:
Article