沉默TREM1改善免疫抑制增强PD-1抑制剂抗肝癌作用及基于调控代谢影响TAM极化的中药活性分子筛选

doi:10.5246/jcps.2026.05.030

中国药学(英文版) ›› 2026, Vol. 35 ›› Issue (5): 420-437.DOI: 10.5246/jcps.2026.05.030

• 【研究论文】 • 上一篇

沉默TREM1改善免疫抑制增强PD-1抑制剂抗肝癌作用及基于调控代谢影响TAM极化的中药活性分子筛选

姚瑞伟¹^,², 曾梓怡¹^,², 何月³^,⁴, 章颖³^,⁴, 钟崇⁵, 张锦芳¹^,²^,^*()

^1. 广州中医药大学深圳医院(福田)肿瘤中心，广东深圳 518000
^2. 广州中医药大学第六临床医学院，广东深圳 518000
^3. 深圳市宝安区中医院，广东深圳 518100
^4. 广州中医药大学第七临床医学院，广东深圳 518100
^5. 中医症候国家重点实验室/广州中医药大学第一附属医院，广东广州 510405

收稿日期:2026-02-15 修回日期:2026-03-24 接受日期:2026-04-16 出版日期:2026-05-31 发布日期:2026-05-31
通讯作者: 张锦芳

Targeting TREM1: screening metabolically-active TCM compounds for TAM polarization and enhancing PD-1 inhibitor efficacy in HCC by alleviating immunosuppression

Ruiwei Yao¹^,², Ziyi Zeng¹^,², Yue He³^,⁴, Ying Zhang³^,⁴, Chong Zhong⁵, Jinfang Zhang¹^,²^,^*()

^1. Cancer Center, Shenzhen Hospital (Futian) of Guangzhou University of Chinese Medicine, Shenzhen 518000, Guangdong, China
^2. The sixth Clinical Medical College, Guangzhou University of Chinese Medicine, Shenzhen 518000, Guangdong, China
^3. Shenzhen Bao’an Chinese Medicine Hospital, Guangzhou University of Chinese Medicine, Shenzhen 518100, Guangdong, China
^4. The seventh Clinical Medical College, Guangzhou University of Chinese Medicine, Shenzhen 518100, Guangdong, China
^5. State Key Laboratory of Traditional Chinese Medicine Syndrome/The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou 510405, Guangdong, China

Received:2026-02-15 Revised:2026-03-24 Accepted:2026-04-16 Online:2026-05-31 Published:2026-05-31
Contact: Jinfang Zhang
Supported by:
National Natural Science Foundation of China (Grant?No. 82575166); Guangzhou University of Chinese Medicine Joint Institutional Scientific and Technological Innovation Fund (Grant?No. GZYFT2024G11) and State Key Laboratory of Integration and Innovation of Classic Formula and Modern Chinese Medicine (Grant?No. LSLSKL20240118).

摘要/Abstract

摘要：

肝癌因其恶性程度高严重影响患者生命健康，免疫治疗逐渐成为肝癌药物治疗的主要手段，免疫抑制性肿瘤微环境常导致肝癌免疫治疗疗效不佳，寻找改善免疫抑制的靶点和药物尤为重要。本研究通过生物信息学分析发现TREM1的表达与肝癌病理进展呈正相关，且高表达TREM1的患者显示了更差的临床预后。此外，TREM1主要表达于巨噬细胞内，并在肿瘤微环境中与巨噬细胞关系最为密切。在体外实验中，敲低TREM1可以抑制肿瘤相关巨噬细胞的免疫抑制表型，且通过小鼠皮下瘤模型证明敲低TREM1与PD-1抑制剂具有协同抗肿瘤作用。RNA测序发现TREM1对代谢相关途径具有调控作用，进一步通过文献分析及分子对接表明代谢相关中药活性成分可能通过靶向TREM1调控TAM代谢发挥抗肝癌作用。本研究有助于为中医药对肝癌的免疫调节提供新的理论依据。

Abstract:

Hepatocellular carcinoma (HCC), characterized by its high malignancy, poses a serious threat to patient survival and health. Immunotherapy has increasingly emerged as a key therapeutic strategy for HCC; however, the immunosuppressive tumor microenvironment (TME) frequently undermines its efficacy. Therefore, identifying molecular targets and therapeutic agents capable of alleviating this immunosuppression is of paramount importance. In this study, bioinformatics analyses revealed that triggering receptor expressed on myeloid cells-1 (TREM1) expression correlated positively with HCC progression, and elevated TREM1 levels were associated with poorer clinical outcomes. Notably, TREM1 was predominantly expressed in macrophages and exhibited the strongest interaction with these cells within the TME. Functional in vitro assays demonstrated that silencing TREM1 attenuated the immunosuppressive phenotype of tumor-associated macrophages (TAMs). In a subcutaneous mouse tumor model, TREM1 knockdown synergized with PD-1 blockade to enhance anti-tumor efficacy. RNA sequencing further indicated that TREM1 modulated metabolism-related pathways. Complementary literature review and molecular docking analyses suggested that specific bioactive compounds derived from traditional Chinese medicine (TCM) might exert anti-HCC effects by targeting TREM1 and regulating TAM metabolism. Collectively, these findings provided a novel mechanistic framework for understanding the immunomodulatory potential of TCM in HCC therapy.

Key words: Hepatocellular carcinoma, Tumor-associated macrophages, Traditional Chinese medicine, PD-1, TREM1, Immunosuppression, Tricarboxylic acid cycle

Supporting:

姚瑞伟, 曾梓怡, 何月, 章颖, 钟崇, 张锦芳. 沉默TREM1改善免疫抑制增强PD-1抑制剂抗肝癌作用及基于调控代谢影响TAM极化的中药活性分子筛选[J]. 中国药学(英文版), 2026, 35(5): 420-437.

Ruiwei Yao, Ziyi Zeng, Yue He, Ying Zhang, Chong Zhong, Jinfang Zhang. Targeting TREM1: screening metabolically-active TCM compounds for TAM polarization and enhancing PD-1 inhibitor efficacy in HCC by alleviating immunosuppression[J]. Journal of Chinese Pharmaceutical Sciences, 2026, 35(5): 420-437.

图/表 11

Table 1. Primer sequence information.

Figure 1. The expression of TREM1 is elevated in tissues from patients with advanced HCC and is associated with a poorer prognosis. (A) Differential expression of TREM1 across the pathological stages of HCC was analyzed using the GEPIA2 database; (B) The association between TREM1 expression and the prognosis of HCC patients was assessed using the GEPIA2 database.

Figure 2. The correlation between TREM1 expression and immune cells within the TME of HCC. Using the TIMER database, we analyzed the correlation between TREM1 expression and the infiltration levels of B cells, CD8CD4+ T cells, CD4+ T cells, macrophages, neutrophils, and dendritic cells in HCC tissues.

Figure 3. The presence of abundant macrophages in HCC tissues is associated with an aggravated adverse prognosis linked to high TREM1 expression. (A) Analysis of TREM1 expression across different cell types in HCC tissues using the TISCH2 single-cell database; (B) Analysis of the association between TREM1 expression and patient prognosis in HCC tissues stratified by high or low macrophage abundance, using the KM Plotter database.

Figure 4. Downregulation of TREM1 inhibits the immunosuppressive phenotype of TAMs. (A) BMDMs were co-cultured with Hepa1-6 CM to generate TAMs. Following knockdown of either NC or TREM1, the expression of immune-suppressive phenotype-related genes in TAMs was analyzed by qRT-PCR; (B) After inducing BMDMs into TAMs and performing knockdown of TREM1 or NC, changes in the secretion of the cytokines TGF-β1 and IL-10 were assessed by ELISA. Compared with si-NC group: *P < 0.05, **P < 0.01, ***P < 0.001.

Figure 5. Inhibiting TREM1 in vivo enhances the anti-tumor efficacy of anti-PD-1 antibodies against HCC. Hepa1-6-luc cells were subcutaneously transplanted into C57BL/6J mice, and siRNA targeting TREM1/NC was used to knockdown TREM1 expression in mice. After treatment with mouse anti-PD-1 antibody, (A) Schematic timeline of the animal experiment; (B) In vivo bioluminescence imaging of the subcutaneous tumor model; (C) Gross appearance of resected tumors; (D) Quantification of tumor volume; (E) Quantification of tumor weight; (F) Representative IHC staining for ARG1 in tumor tissues; (G) Representative IHC staining for CD206 in tumor tissues. Compared with si-NC group: *P < 0.05, **P < 0.01, ***P < 0.001. Compared with si-TREM1+PD-1 group: #P < 0.05, ##P < 0.01, ###P < 0.001.

Figure 6. Assessment of safety following combination treatment with si-TREM1 and anti-PD-1 antibody. Subcutaneous transplantation of Hepa1-6-luc cells was performed in C57BL/6J mice, and siRNA targeting TREM1/NC was used to deplete TREM1 expression in animals. After treatment with mouse anti-PD-1 antibody, (A) Body weight statistics graph of mice, (B) H&E staining of liver tissue, (C) H&E staining of kidney tissue.

Figure 7. Transcriptome sequencing indicates that depletion of TREM1 affects the metabolism of TAMs. Transcriptome sequencing and analysis were conducted on TAMs with knocked-down NC/TREM1. (A) Volcano plot of DEGs; (B) GO enrichment analysis diagram; (C) KEGG enrichment analysis diagram; (D) GSEA diagram.

Table 2. A summary of TCM active components with metabolic regulatory functions over the past 3 years.

Table 3. Molecular docking results.

Figure 8. Molecular docking screening of active components from TCM that may target TREM1 to modulate TAM metabolism. Molecular docking results for the interaction between the TREM1 protein and the TCM active compounds Tanshinone IIA, Luteolin, Quercetin, and Icariin.

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沉默TREM1改善免疫抑制增强PD-1抑制剂抗肝癌作用及基于调控代谢影响TAM极化的中药活性分子筛选

Targeting TREM1: screening metabolically-active TCM compounds for TAM polarization and enhancing PD-1 inhibitor efficacy in HCC by alleviating immunosuppression

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