Zhao Feng, An Rui, Ma Yilei, Yu Shaobo, Gao Yuzhen, Wang Yanzhong, Yu Haitao, Xie Xinyou, Zhang Jun
Department of Clinical Laboratory, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, People's Republic of China.
Key Laboratory of Precision Medicine in Diagnosis and Monitoring Research of Zhejiang Province, Hangzhou, Zhejiang, People's Republic of China.
Clin Transl Med. 2025 Mar;15(3):e70273. doi: 10.1002/ctm2.70273.
Tumour-associated microbiota are integral components of the tumour microenvironment (TME). However, previous studies on intratumoral microbiota primarily rely on bulk tissue analysis, which may obscure their spatial distribution and localized effects. In this study, we applied in situ spatial-profiling technology to investigate the spatial distribution of intratumoral microbiota in breast cancer and their interactions with the local TME. Using 5R 16S rRNA gene sequencing and RNAscope FISH/CISH on patients' tissue, we identified significant spatial heterogeneity in intratumoral microbiota, with Fusobacterium nucleatum (F. nucleatum) predominantly localized in tumour cell-rich areas. GeoMx digital spatial profiling (DSP) revealed that regions colonized by F. nucleatum exhibit significant influence on the expression of RNAs and proteins involved in proliferation, migration and invasion. In vitro studies indicated that co-culture with F. nucleatum significantly stimulates the proliferation and migration of breast cancer cells. Integrative spatial multi-omics and co-culture transcriptomic analyses highlighted the MAPK signalling pathways as key altered pathways. By intersecting these datasets, VEGFD and PAK1 emerged as critical upregulated proteins in F. nucleatum-positive regions, showing strong positive correlations with MAPK pathway proteins. Moreover, the upregulation of VEGFD and PAK1 by F. nucleatum was confirmed in co-culture experiments, and their knockdown significantly reduced F. nucleatum-induced proliferation and migration. In conclusion, intratumoral microbiota in breast cancer exhibit significant spatial heterogeneity, with F. nucleatum colonization markedly altering tumour cell protein expression to promote progression and migration. These findings provide novel perspectives on the role of microbiota in breast cancer, identify potential therapeutic targets, and lay the foundation for future cancer treatments. KEY POINTS: Intratumoral Fusobacterium nucleatum exhibits significant spatial heterogeneity within breast cancer tissues. F. nucleatum colonization alters the expression of key proteins involved in tumour progression and migration. The MAPK signalling pathway is a critical mediator of F. nucleatum-induced breast cancer cell proliferation and migration. VEGFD and PAK1 are potential therapeutic targets to mitigate F. nucleatum-induced tumour progression.
肿瘤相关微生物群是肿瘤微环境(TME)的重要组成部分。然而,先前关于肿瘤内微生物群的研究主要依赖于大块组织分析,这可能会掩盖它们的空间分布和局部效应。在本研究中,我们应用原位空间分析技术来研究乳腺癌肿瘤内微生物群的空间分布及其与局部TME的相互作用。通过对患者组织进行5R 16S rRNA基因测序和RNAscope FISH/CISH,我们发现肿瘤内微生物群存在显著的空间异质性,具核梭杆菌(F. nucleatum)主要定位于肿瘤细胞丰富的区域。GeoMx数字空间分析(DSP)显示,被具核梭杆菌定殖的区域对参与增殖、迁移和侵袭的RNA和蛋白质表达有显著影响。体外研究表明,与具核梭杆菌共培养可显著刺激乳腺癌细胞的增殖和迁移。综合空间多组学和共培养转录组分析突出了MAPK信号通路是关键的改变通路。通过交叉分析这些数据集,VEGFD和PAK1成为具核梭杆菌阳性区域中关键的上调蛋白,与MAPK通路蛋白呈强正相关。此外,在共培养实验中证实了具核梭杆菌对VEGFD和PAK1的上调作用,敲低它们可显著降低具核梭杆菌诱导的增殖和迁移。总之,乳腺癌肿瘤内微生物群表现出显著的空间异质性,具核梭杆菌定殖显著改变肿瘤细胞蛋白表达以促进进展和迁移。这些发现为微生物群在乳腺癌中的作用提供了新的视角,确定了潜在的治疗靶点,并为未来的癌症治疗奠定了基础。要点:肿瘤内具核梭杆菌在乳腺癌组织中表现出显著的空间异质性。具核梭杆菌定殖改变了参与肿瘤进展和迁移的关键蛋白的表达。MAPK信号通路是具核梭杆菌诱导乳腺癌细胞增殖和迁移的关键介质。VEGFD和PAK1是减轻具核梭杆菌诱导的肿瘤进展的潜在治疗靶点。