Dataset related to article"Integrating single-cell and spatial transcriptomics to elucidate the crosstalk between cancer-associated fibroblasts and cancer cells in hepatocellular carcinoma with spleen-deficiency syndrome"

Most patients with hepatocellular carcinoma (HCC) in China have been diagnosed with spleen deficiency syndrome (SDS), which accelerates the progression of HCC by disrupting the tumor microenvironment (TME) homeostasis. However, the underlying mechanism remains to be explored. By integrating single-cell and spatial transcriptomics, we found that the crosstalk between CAFs and cancer cells is crucial for the tumor-promoting effect of SDS. CAFs recruited by HCC via PDGFA may lead to ECM remodeling through activation of the TGF-β pathway, thereby forming a physical barrier to block immune cell infiltration under SDS.在中国，绝大多数肝细胞癌（hepatocellular carcinoma, HCC）患者均被确诊为脾虚证（spleen deficiency syndrome, SDS），该证型通过破坏肿瘤微环境（tumor microenvironment, TME）稳态加速HCC进展。然而，其潜在作用机制尚待阐明。本研究通过整合单细胞与空间转录组学技术，发现癌相关成纤维细胞（cancer-associated fibroblasts, CAFs）与肿瘤细胞间的交互串扰，在SDS的促肿瘤效应中发挥关键作用。HCC可通过血小板源性生长因子A（platelet-derived growth factor A, PDGFA）招募CAFs，后者可通过激活转化生长因子-β（transforming growth factor-β, TGF-β）通路介导细胞外基质（extracellular matrix, ECM）重塑，进而形成物理屏障，阻断SDS状态下免疫细胞的浸润。