PTPN2 induced by inflammatory response and oxidative stress contributed to glioma progression.
J Cell Biochem
; 120(11): 19044-19051, 2019 11.
Article
em En
| MEDLINE
| ID: mdl-31241223
ABSTRACT
Malignant glioma remains the most frequent form of primary brain tumors all over the world. The gliomagenesis is characterized by various molecular processes such as neoplastic transformation, dysregulation of the cell cycle, and angiogenesis. Among these biomolecular events, the existence of inflammation and oxidative stress pathways in the development of glioma has been reported. PTPN2 is associated with several inflammatory disorders. However, the biological role of PTPN2 in inflammation responses and oxidative stress pathways involved in glioma remains poorly known. Here, we focused on its function in glioma development. Here, we observed that PTPN2 was significantly increased in glioma especially in a grade-dependent manner. Meanwhile, interferon-γ and tumor necrosis factor-α, which have been identified as crucial inflammation cytokines, were able to trigger PTPN2 expression in a dose-dependent course in T98G cells. Then, we found that PTPN2 was oxidated and inactivated by H2 O2 . Meanwhile, H2 O2 induced glioma cell colony formation capacity and increased ki-67 expression confirmed by flow cytometry assay. Finally, T98G cells were transfected with PTPN2 shRNA and it was shown that knockdown of PTPN2 obviously inhibited T98G cell colony formation and induced cell apoptosis. In summary, our findings indicated that PTPN2 could be induced by inflammatory response and oxidative stress and its deficiency depressed glioma cell growth.
Palavras-chave
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Estresse Oxidativo
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Proteína Tirosina Fosfatase não Receptora Tipo 2
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Glioma
Tipo de estudo:
Prognostic_studies
Limite:
Animals
/
Humans
Idioma:
En
Revista:
J Cell Biochem
Ano de publicação:
2019
Tipo de documento:
Article
País de afiliação:
China