癌症研究
胶质母细胞瘤
化疗
PI3K/AKT/mTOR通路
基因敲除
医学
U87型
替莫唑胺
免疫组织化学
下调和上调
细胞培养
免疫印迹
信号转导
生物
病理
内科学
细胞生物学
基因
遗传学
生物化学
标识
DOI:10.1016/j.amjms.2018.06.019
摘要
Background The clinical management of glioblastoma is still challenging despite aggressive surgery and radio-chemotherapy approaches. Better understanding of the molecules involved in glioblastoma chemoresistance is necessary to improve the treatment and predict prognosis. Materials and Methods We analyzed the expression and possible roles of cytosolic phospholipase A2 alpha (cPLA2α) in human glioblastoma cell lines and patient samples using immunohistochemistry and cellular assays. We analyzed the signaling pathways that cPLA2α regulates in glioblastoma cells using western blot analysis. Results Our work demonstrated that cPLA2α is upregulated in glioblastoma compared with normal neuron cells. The expression of cPLA2α varies in multiple glioblastoma cell lines and is associated with chemoresistance rather than tumor development. cPLA2α depletion moderately inhibits glioblastoma growth and survival but remarkably sensitizes chemo-resistant glioblastoma cells to several chemotherapeutic agents. Mechanistically, cPLA2α knockdown significantly suppresses the PI3K/Akt/mTOR pathway in glioblastoma cells. Conclusions We are the first to identify the important role of cPLA2α in glioblastoma in response to chemotherapy. Our data also suggest that cPLA2α may serve as a biomarker to indicate prognosis of glioblastoma patients with high level of cPLA2α to chemotherapy.
科研通智能强力驱动
Strongly Powered by AbleSci AI