肿瘤炎症微环境在癌症（特别是前列腺癌）进展中的作用已得到广泛认可。 ELL 相关因子 2 (EAF2) 是一种在前列腺中发现的肿瘤抑制因子，在前列腺癌中经常下调。早期的研究表明，EAF2基因敲除的小鼠表现出大量炎症细胞浸润到前列腺基质中。选择了由38名被诊断患有前列腺癌并随后接受根治性前列腺切除术（RP）的患者组成的队列。根据格里森评分系统对这些患者进行病理分级并分为两组。此选择的目的是使用免疫组织化学 (IHC) 染色研究 EAF2 和 CD163 之间的潜在相关性。此外，我们还进行了体外实验来验证EAF2表达与巨噬细胞迁移和极化之间的关系。我们的研究表明，在人类前列腺癌标本中，EAF2的表达显着下调，并且这种下调与CD163的数量呈负相关。 - 浸润癌组织的阳性巨噬细胞。细胞共培养实验表明，当EAF2被敲除时，肿瘤细胞对巨噬细胞的趋化作用增强，并且巨噬细胞分化为肿瘤相关巨噬细胞（TAM）。此外，细胞因子蛋白微阵列的应用显示，EAF2敲除后趋化因子巨噬细胞迁移抑制因子（MIF）的表达增加。我们的研究结果表明，EAF2通过MIF参与前列腺癌中CD163阳性巨噬细胞的浸润。© 2024。作者。

The role of tumor inflammatory microenvironment in the advancement of cancer, particularly prostate cancer, is widely acknowledged. ELL-associated factor 2 (EAF2), a tumor suppressor that has been identified in the prostate, is often downregulated in prostate cancer. Earlier investigations have shown that mice with EAF2 gene knockout exhibited a substantial infiltration of inflammatory cells into the prostatic stroma.A cohort comprising 38 patients who had been diagnosed with prostate cancer and subsequently undergone radical prostatectomy (RP) was selected. These patients were pathologically graded according to the Gleason scoring system and divided into two groups. The purpose of this selection was to investigate the potential correlation between EAF2 and CD163 using immunohistochemistry (IHC) staining. Additionally, in vitro experimentation was conducted to verify the relationship between EAF2 expression, macrophage migration and polarization.Our study demonstrated that in specimens of human prostate cancer, the expression of EAF2 was notably downregulated, and this decrease was inversely associated with the number of CD163-positive macrophages that infiltrated the cancerous tissue. Cell co-culture experiments revealed that the chemotactic effect of tumor cells towards macrophages was intensified and that macrophages differentiated into tumor-associated macrophages (TAMs) when EAF2 was knocked out. Additionally, the application of cytokine protein microarray showed that the expression of chemokine macrophage migration inhibitory factor (MIF) increased after EAF2 knockout.Our findings suggested that EAF2 was involved in the infiltration of CD163-positive macrophages in prostate cancer via MIF.© 2024. The Author(s).