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ANXA5 promotes glioma progression through the FAk/PI3K/AKT pathway

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Abstract Objective Annexin A5 (ANXA5) is a member of the calcium dependent phospholipid binding protein family and participates in the regulation of a variety of physiological and pathological processes. However, whether and how ANXA5 affects the growth and progression of glioma remains unclear. Methods We analyzed the expression of ANXA5 in multiple public databases, and verified the expression in 50 glioma clinical samples with Western blotting to study the correlation between ANXA5 and prognosis, survival, and clinical characteristics. In vitro experiments, we up-regulated and down-regulated the expression of ANXA5 in glioma cells, then treated glioma cells with up regulated ANXA5 expression with Y397 FAK specific phosphorylation inhibitor Y15, and verified the effect of ANXA5 on proliferation, migration and invasion of glioma cells through CCK8, clone formation, EDU, mgration and invasion assays, scratching,and Western blotting proved that the expression level of ANXA5 affected the protein level of upstream and downstream factors of FAk/PI3K/AK pathway. Results ANXA5 is highly expressed in glioma and is related to clinical features such as grade, age and molecular typing. The higher the expression of ANXA5, the worse the prognosis. The increased expression of ANXA5 can promote the proliferation, migration and invasion of glioma cells, activate FAk/PI3K/AK pathway, and Y15 can reverse the promotion of ANXA5 overexpression; When ANXA5 is knocked down, the result is opposite. Conclusions ANXA5 is highly expressed in glioma and is an independent prognostic factor of glioma patients. ANXA5 can promote the proliferation, migration and invasion of glioma cells through FAk/PI3K/AK pathway, and this promotion can be reversed by Y15.
Title: ANXA5 promotes glioma progression through the FAk/PI3K/AKT pathway
Description:
Abstract Objective Annexin A5 (ANXA5) is a member of the calcium dependent phospholipid binding protein family and participates in the regulation of a variety of physiological and pathological processes.
However, whether and how ANXA5 affects the growth and progression of glioma remains unclear.
Methods We analyzed the expression of ANXA5 in multiple public databases, and verified the expression in 50 glioma clinical samples with Western blotting to study the correlation between ANXA5 and prognosis, survival, and clinical characteristics.
In vitro experiments, we up-regulated and down-regulated the expression of ANXA5 in glioma cells, then treated glioma cells with up regulated ANXA5 expression with Y397 FAK specific phosphorylation inhibitor Y15, and verified the effect of ANXA5 on proliferation, migration and invasion of glioma cells through CCK8, clone formation, EDU, mgration and invasion assays, scratching,and Western blotting proved that the expression level of ANXA5 affected the protein level of upstream and downstream factors of FAk/PI3K/AK pathway.
Results ANXA5 is highly expressed in glioma and is related to clinical features such as grade, age and molecular typing.
The higher the expression of ANXA5, the worse the prognosis.
The increased expression of ANXA5 can promote the proliferation, migration and invasion of glioma cells, activate FAk/PI3K/AK pathway, and Y15 can reverse the promotion of ANXA5 overexpression; When ANXA5 is knocked down, the result is opposite.
Conclusions ANXA5 is highly expressed in glioma and is an independent prognostic factor of glioma patients.
ANXA5 can promote the proliferation, migration and invasion of glioma cells through FAk/PI3K/AK pathway, and this promotion can be reversed by Y15.

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