本研究探讨了乳酸在卵巢癌（OV）发生和进展中的作用，并探讨其潜在机制。 OV患者的血清乳酸水平与肿瘤分级和不良预后呈正相关。生物信息学分析将 CCL18 鉴定为 OV 中的乳酸相关基因。 CCL18 在癌组织中表达上调，并且与 OV 患者的血清乳酸水平呈正相关。 THP-1 细胞暴露于 phorbol-12-myristate-13-acetate 以诱导 M0 巨噬细胞。 M1/M2 巨噬细胞相关标记物和炎症细胞因子的 RT-qPCR 和 ELISA 结果表明，巨噬细胞接触乳酸会诱导 M2 极化。基于OV细胞与巨噬细胞的共培养，乳酸处理的巨噬细胞诱导OV细胞的增殖和迁移显着增加。然而，这些效应可以通过巨噬细胞中 Gpr132 的沉默或用抗 CCL18 抗体治疗来逆转。使用异种移植模型的实验验证了乳酸在肿瘤生长和转移中的致癌作用依赖于Gpr132和CCL18。 ChIP-qPCR 和荧光素酶报告基因检测表明，乳酸通过 H3K18 乳酰化调节 CCL18 表达。总之，乳酸是 OV 的潜在治疗靶点。它通过巨噬细胞中的 H3K18 乳酰化激活 CCL18 表达，从而参与肿瘤发生。

This study investigates the role of lactate in the genesis and progression of ovarian cancer (OV) and explores the underlying mechanisms. Serum lactate levels show a positive correlation with tumor grade and poor prognosis in patients with OV. Bioinformatics analysis identifies CCL18 as a lactate-related gene in OV. CCL18 is up-regulated in cancerous tissues and positively related to serum lactate levels in OV patients. THP-1 cells are exposed to phorbol-12-myristate-13-acetate for M0 macrophage induction. The results of RT-qPCR and ELISA for M1/M2 macrophage-related markers and inflammatory cytokines show that the exposure of lactate to macrophages induces M2 polarization. Based on the coculture of OV cells with macrophages, lactate-treated macrophages induces a significant increase in the proliferation and migration of OV cells. However, these effects can be reversed by silencing of Gpr132 in macrophages or treatment with anti-CCL18 antibody. Experiments using the xenograft model verify that the oncogenic role of lactate in tumor growth and metastasis relies on Gpr132 and CCL18. ChIP-qPCR and luciferase reporter assays reveal that lactate regulates CCL18 expression via H3K18 lactylation. In conclusion, lactate is a potential therapeutic target for OV. It is involved in tumorigenesis by activating CCL18 expression via H3K18 lactylation in macrophages.