ALOX5 induces EMT and promotes cell metastasis via the LTB4/BLT2/PI3K/AKT pathway in ovarian cancer

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 si...

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Bibliographic Details
Published in:Cellular signalling 2024-12, Vol.124, p.111404, Article 111404
Main Authors: Ji, Zhaodong, Li, Xiaoqi, Gao, Wen, Xia, Qiuyi, Li, Jiwei
Format: Article
Language:English
Subjects:
ALOX5
Arachidonate 5-Lipoxygenase - genetics
Arachidonate 5-Lipoxygenase - metabolism
Cadherins - metabolism
Cell Line, Tumor
Cell Movement
EMT
Epithelial-Mesenchymal Transition
Female
Gene Expression Regulation, Neoplastic
Humans
Leukotriene B4 - metabolism
Metastasis
Neoplasm Metastasis
Ovarian cancer
Ovarian Neoplasms - genetics
Ovarian Neoplasms - metabolism
Ovarian Neoplasms - pathology
Phosphatidylinositol 3-Kinases - metabolism
Proto-Oncogene Proteins c-akt - metabolism
Receptors, Leukotriene B4
Signal Transduction
Snail Family Transcription Factors - genetics
Snail Family Transcription Factors - metabolism
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Summary: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. •ALOX5 is implicated in EMT in ovarian cancer.•ALOX5 promoted EMT and cancer metastasis through PI3K/AKT pathway, whereas SNAI1 inhibited the transcription of CDH1 in OC cells.•Our study provides novel strategies for the prevention of metastasis in ovarian cancer.
ISSN:0898-6568
1873-3913
1873-3913
DOI:10.1016/j.cellsig.2024.111404