转移
PI3K/AKT/mTOR通路
卵巢癌
癌症研究
蛋白激酶B
上皮-间质转换
细胞迁移
癌症
下调和上调
基因沉默
癌细胞
化学
生物
细胞
医学
内科学
信号转导
细胞生物学
生物化学
基因
作者
Zhaodong Ji,Xiaoqi Li,Wen Gao,Qiuyi Xia,Jiwei Li
标识
DOI:10.1016/j.cellsig.2024.111404
摘要
Ovarian cancer represents the most lethal gynecological malignancy with high invasiveness. Epithelial-to-mesenchymal transition (EMT) plays a critical role in cancer metastasis. However, the role of ALOX5 in EMT and cancer metastasis in ovarian cancer (OC) remain unclear. In this study, ALOX5 was significantly upregulated in tumorous and metastatic tissue compared with normal tissue. Furthermore, we found that overexpression of ALOX5 promoted cell migration and invasion, while silencing of ALOX5 suppressed migration and invasion in OC cell lines. Mechanistically, we found that enhanced expression of ALOX5 promoted EMT and cancer metastasis through activation of the PI3K/AKT pathway, whereas SNAIl inhibited the transcription of CDH1 in OC cells. Taken together, our results highlight a role for the ALOX5/PI3K/AKT/ SNAI1 axis in OC, which provides novel strategies for the prevention of metastasis in OC.
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