ALOX5 通过 LTB4/BLT2/PI3K/AKT 通路诱导卵巢癌 EMT 并促进细胞转移

IF 4.4 2区生物学 Q2 CELL BIOLOGY

Cellular signalling Pub Date : 2024-09-08 DOI:10.1016/j.cellsig.2024.111404

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引用次数: 0

摘要

卵巢癌是致死率最高的妇科恶性肿瘤，具有高度侵袭性。上皮细胞向间质转化（EMT）在癌症转移中起着关键作用。然而，ALOX5在卵巢癌（OC）EMT和癌症转移中的作用仍不清楚。本研究发现，与正常组织相比，ALOX5 在肿瘤组织和转移组织中明显上调。此外，我们发现过表达 ALOX5 会促进细胞迁移和侵袭，而沉默 ALOX5 则会抑制 OC 细胞株的迁移和侵袭。从机理上讲，我们发现 ALOX5 的表达增强可通过激活 PI3K/AKT 通路促进 EMT 和癌症转移，而 SNAIl 可抑制 OC 细胞中 CDH1 的转录。综上所述，我们的研究结果凸显了ALOX5/PI3K/AKT/ SNAI1轴在OC中的作用，这为预防OC转移提供了新的策略。

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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 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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来源期刊

Cellular signalling 生物-细胞生物学

CiteScore

8.40

自引率

0.00%

发文量

250

审稿时长

27 days

期刊介绍： Cellular Signalling publishes original research describing fundamental and clinical findings on the mechanisms, actions and structural components of cellular signalling systems in vitro and in vivo. Cellular Signalling aims at full length research papers defining signalling systems ranging from microorganisms to cells, tissues and higher organisms.