| 孔维娜,马佳雪,郭凡,等.TREM2调控M2型TAMs极化促进宫颈癌进展的机制研究[J].安徽医药,待发表. |
| TREM2调控M2型TAMs极化促进宫颈癌进展的机制研究 |
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| 投稿时间：2026-04-02 录用日期：2026-05-06 |
| DOI： |
| 中文关键词: 髓系细胞触发受体2 M2型肿瘤相关巨噬细胞 宫颈癌 脂肪酸结合蛋白 |
| 英文关键词: |
| 基金项目:新疆医科大学医学科学研究所开放课题资助项目(YXYJ20240302)；自治区卫生健康青年医学科技人才专项科研项目(WJWY-202403)；新疆维吾尔自治区自然科学基金资助项目(2022D01C507) |
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| 中文摘要: |
| 目的 髓系细胞触发受体2（Triggering receptor expressed on myeloid cells 2, TREM2）在肿瘤微环境中主要表达在肿瘤相关巨噬细胞（tumor-associated macrophages, TAMs）上，其中，M2型TAMs在宫颈癌中主要发挥免疫抑制作用。本研究旨在探讨TREM2是否能够调控脂质代谢分子影响TAMs的表型和功能，为此以TREM2为靶点的肿瘤免疫治疗提供一定的理论依据。方法 收集宫颈癌患者临床资料和病理组织，利用免疫组织化学对TREM2染色。通过慢病毒敲低或过表达M2型TAMs上TREM2后，检测TREM2、脂质代谢相关分子（FABP4、FABP5、FASN）及TAMs特征性分子表达。通过CCK8和Transwell迁移实验观察TREM2对宫颈癌细胞功能的影响。结果 宫颈癌患者中TREM2表达高于对照组。M2型较M1型TAMs高表达TREM2、FABP4、FABP5及FASN。敲低TREM2后，发现FABP4、FABP5、FASN及M2型TAMs特征性分子表达降低，宫颈癌细胞的增殖和迁移功能减弱，过表达结果相反。结论 宫颈癌微环境中TAMs中TREM2可能通过调控相关脂质代谢分子，促进其向M2型抑炎型极化，从而加快宫颈癌的进展。因此，以TREM2为靶点的肿瘤免疫治疗可能是一种新的治疗策略。 |
| 英文摘要: |
| Objective Triggering receptor expressed on myeloid cells 2 (TREM2) is mainly expressed on tumor-associated macrophages (TAMs) in the tumor microenvironment. Notably, M2-type TAMs predominantly exert an immunosuppressive effect in cervical cancer. This study aims to investigate whether TREM2 can regulate lipid metabolism molecules to influence the phenotype and function of TAMs, thereby providing a certain theoretical basis for tumor immunotherapy targeting TREM2. Methods Clinical data and pathological tissues of cervical cancer patients were collected, and TREM2 was stained by immunohistochemistry. Following the knockdown or overexpression of TREM2 in M2-type TAMs using lentiviral vectors, we assessed the expression levels of TREM2, lipid metabolism-related molecules (including FABP4, FABP5, and FASN), as well as characteristic markers of TAMs. Furthermore, the impact of TREM2 on the functional behavior of cervical cancer cells was evaluated through CCK8 and Transwell migration assays. Results The expression level of TREM2 is elevated in cervical cancer patients in comparison to the control group. M2-type TAMs exhibited higher expression of TREM2, FABP4, FABP5 and FASN compared to M1-type TAMs. After knockdown of TREM2, it was found that the expressions of FABP4, FABP5, FASN and the characteristic molecules of M2-type TAMs decreased, and the proliferation and migration functions of cervical cancer cells weakened. Conversely, overexpression yielded opposite effects. Conclusions In the microenvironment of cervical cancer, TREM2 in TAMs may promote their polarization towards the M2 anti-inflammatory phenotype by regulating related lipid metabolism molecules, thereby accelerating the progression of cervical cancer. Therefore, tumor immunotherapy targeting TREM2 may be a new therapeutic strategy. |
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