三阴性乳腺癌（TNBC）的治疗选择有限。中医药在TNBC的治疗中发挥着重要作用。半枝莲 (Scutellaria barbata D.Don) 和 Scleromitrion diffusum (Willd.) R.J.Wang (SH) 草药对因其抗肿瘤特性而常用于临床实践。已被证明对肿瘤相关疾病具有良好的治疗效果，但其潜在的分子机制尚未完全阐明。通过生物信息学验证，IL6主要来源于癌症相关成纤维细胞（CAFs），与肿瘤相关的不良预后相关。预后。此外，细胞和动物实验证实SH通过抑制IL6/NF-κB通路来抑制原位肿瘤模型中的肿瘤增殖、迁移和生长。使用GEO、TCGA和HPA数据库分析CAF和IL6的预后价值，然后检测到IL6资源。经过生物信息学分析，通过体外和体内实验验证了CAFs和CAFs衍生的IL6对TNBC的影响。采用细胞克隆形成实验、伤口愈合实验和Transwell实验检测体外对CAFs和CAFs衍生IL6的促进作用以及对SH的抑制作用。利用小鼠TNBC模型证明了CAFs和CAFs衍生的IL6在体内的促进作用和SH的抑制作用。通过检测独特的分子，通过蛋白质印迹探索NF-κB的生物学通路。生物信息学分析显示，较高比例的CAF和升高的IL6水平与TNBC不良预后显着相关。同时，IL6被证明主要来源于CAF。经过生物信息学的指示，体外实验证明CAFs和IL6均能增强MDA-MD-231细胞的克隆形成和迁移能力(231)，而且CAFs的促进作用与IL6的水平有关。基于这些数据，发现CAFs来源的IL6增强与NF-κB信号通路的激活密切相关，而SH可以降低该激活。最终，CAFs/CAFs衍生的IL6/NF-κB的促进作用和SH抑制的功效均通过体内实验得到证实。生物信息学数据表明，较高的CAFs比例与较高水平的CAFs衍生的IL6显着相关。 TNBC 的生存率较差。 CAFs和CAFs衍生的IL6在体外和体内均被证明可促进TNBC的进展，且该过程与NF-κB的激活显着相关。 SH抑制TNBC的进展，并被证明与CAFs/CAFs衍生的IL6/NF-κB密切相关。版权所有©2024 Elsevier B.V.保留所有权利。

The treatment options for triple-negative breast cancer (TNBC) are limited. Traditional Chinese Medicine (TCM) plays an important role in the treatment of TNBC. The herb pair Scutellaria barbata D.Don and Scleromitrion diffusum (Willd.) R.J.Wang (SH) is commonly used in clinical practice for its anti-tumor properties. It has been proven to have good therapeutic effects on tumor-related diseases, but the underlying molecular mechanisms are not yet fully explained.Through bioinformatics, it was validated that IL6, primarily derived from cancer-associated fibroblasts (CAFs), is associated with poor prognosis. Additionally, cell and animal experiments confirmed that SH inhibits tumor proliferation, migration, and growth in an orthotopic tumor model by suppressing the IL6/NF-κB pathway.GEO, TCGA and HPA databases were used to analyze the prognostic value of CAFs and IL6, then IL6 resource was detected. After the bioinformatics, the influence of CAFs and CAFs-derived IL6 on TNBC was verified by experiments both in vitro and in vivo. Cell clone formation assay, wound-Healing assay, and Transwell assay were used to detect the promotion of CAFs and CAFs-derived IL6 and the inhibition of SH in vitro. TNBC model in mice was used to prove the promotion of CAFs and CAFs-derived IL6 and the inhibition of SH in vivo. The biological pathway of NF-κB was explored by western blotting through detecting unique molecules.Bioinformatics analysis revealed that higher proportion of CAFs and elevated level of IL6 were significantly associated with poor prognosis in TNBC. At the same time, IL6 was proved predominantly derived from CAFs. After the indication of bioinformatics, experiments in vitro demonstrated that both CAFs and IL6 could enhance the clone formation and migration ability of MDA-MD-231 cells (231), furthermore, the promotion of CAFs was related with the level of IL6. Based on these data, mechanism was detected that CAFs-derived IL6 enhancement was closely related to the activation of NF-κB signaling pathway, while the activation can be reduced by SH. In the end, the promotion of CAFs/CAFs-derived IL6/NF-κB and the efficacy of SH inhibition were both confirmed by experiments in vivo.Bioinformatics data indicates that higher proportion of CAFs and higher level of CAFs-derived IL6 are significantly related to poorer survival of TNBC. CAFs and CAFs-derived IL6 were proved to promote the progression of TNBC both in vitro and in vivo, and the process of which was significantly related to the activation of NF-κB. SH inhibited the progress of TNBC, which was proved to be closely related to CAFs/CAFs-derived IL6/NF-κB.Copyright © 2024 Elsevier B.V. All rights reserved.