肿瘤干细胞是具有自我更新能力和分化潜能的肿瘤细胞。卵巢癌干细胞是卵巢癌生长、转移和复发的根源，其干性的维持受细胞因子和趋化因子及其受体的调控。抗炎促消退介质脂氧素A4(LXA4)可通过活化其受体ALX/FPR2，负性调节STAT3和NF-κB等炎症及肿瘤发生相关的信号通路，显著抑制肿瘤细胞分泌炎症因子、增殖和转移，促进肿瘤细胞凋亡。我们预实验结果显示ALX/FPR2在卵巢癌干细胞表达，LXA4可下调干细胞标志Oct4和CD133的表达，提示ALX/FPR2可能直接参与肿瘤细胞干性的调控。本课题旨在系统阐明ALX/FPR2对卵巢癌干细胞自我更新、分化和侵袭转移的调控机制，为丰富肿瘤病理生理学和肿瘤干细胞理论做贡献，为抗癌治疗策略的制定提供新线索。

Cancer stem cells (CSCs) are a subpopulation of cancer cells with capabilities of self-renewal and differentiation. Ovarian CSCs are the root cause of growth, metastasis and recurrence of the ovarian cancer. The stemness maintenance of them is regulated by cytokines and chemokines and their receptors. The anti-inflammatory and proresolving mediator lipoxin A4 (LXA4), by activating its receptor ALX/FPR2, negatively regulates the inflammation and cancer related signalings such as STAT3 and NF-κB pathways, significantly inhibits the secretion of inflammatory factors, proliferation and metastasis of cancer cells, promotes cancer cell apoptosis. Our previous studies demonstrated the expression of ALX/FPR2 in ovarian CSCs. The stem cell markers Oct4 and CD133 were downregulated by LXA4, suggesting that ALX/FPR2 might directly regulates the stemness of CSCs. This study intends to elucidate the regulatory mechanisms of ALX/FPR2 on the self-renewal, differentiation, invasion and metastasis of ovarian CSCs. This study will enrich the theories of cancer pathophysiology and CSCs,and provide new clues for the development of anti-cancer therapeutic strategies.