Supplementary Table S3 from CD36+ Proinflammatory Macrophages Interact with ZCCHC12+ Tumor Cells in Papillary Thyroid Cancer Promoting Tumor Progression and Recurrence
posted on 2024-11-04, 08:21authored byXin Zhang, Limei Guo, Wenyu Tian, Ying Yang, Yue Yin, Yaruo Qiu, Weixuan Wang, Yang Li, Guangze Zhang, Xuyang Zhao, Guangxi Wang, Zhiqiang Lin, Meng Yang, Wei Zhao, Dan Lu
Supplementary Table S3 Comparative p-values for PFS rate and DFS rate in high infiltration group and low-infiltration group, stratified using different cellular characteristics in TCGA.
Funding
Natural Science Foundation of Beijing Municipality (Beijing Natural Science Foundation)
National Natural Science Foundation of China (NSFC)
Fundamental Research Funds for the Central Universities (Fundamental Research Fund for the Central Universities)
Beijing Municipal Science and Technology Commission, Administrative Commission of Zhongguancun Science Park
History
ARTICLE ABSTRACT
Local recurrence and distal metastasis negatively impact the survival and quality of life in patients with papillary thyroid cancer (PTC). Therefore, identifying potential biomarkers and therapeutic targets for PTC is clinically crucial. In this study, we performed a multiomics analysis that identified a subset of CD36+ proinflammatory macrophages within the tumor microenvironment of PTC. The recruitment of CD36+ macrophages to premalignant regions strongly correlated with unfavorable outcomes in PTC, and the presence of tumor-infiltrating CD36+ macrophages was determined to be a risk factor for recurrence. The CD36+ macrophages exhibited interactions with metabolically active ZCCHC12+ tumor cells. By secreting SPP1, the CD36+ macrophages activated the PI3K-AKT signaling pathway, thereby promoting proliferation of the cancer cells. Dysregulation of iodine metabolism was closely related to the acquisition of the pro-inflammatory phenotype in macrophages. Iodine supplementation inhibited the activation of proinflammatory signaling and impeded the development of CD36+ macrophages by enhancing DUSP2 expression. Overall, our findings shed light on the intricate cross-talk between CD36+ macrophages and ZCCHC12+ tumor cells, providing valuable insights for the treatment and prognosis of PTC.