Liver metastasis (LM) frequently occurs in patients with advanced lung cancer; yet our understanding of the underlying salient biology is preliminary. Here, we performed single-cell RNA-seq in three patients with LM of lung cancer and compared them with the single-cell RNA-seq of hepatocellular carcinoma and primary lung cancer in public database.
Single cell RNA sequencing was performed on tissues from LM of lung cancer. Also, we downloaded the single-cell RNA-seq of hepatocellular carcinoma and primary lung cancer from TCGA and GEO database. We applied Seurat to sort single-cell RNA-seq of LM in lung cancer and primary lung cancer into different clusters via feature dimension reduction and then investigated their expression profiling, stemness initiating and enrichment pathways. Furthermore, CellChat was used to compare the cellular communication and regulatory network of tumor microenvironment among LM of lung cancer, hepatocellular carcinoma, and primary lung cancer.
33820, 23427, 21750 tumor cells among LM in lung cancer, hepatocellular carcinoma, and primary lung cancer were extracted respectively. There were 30 clusters divided into LM of lung cancer and primary lung cancer and cluster 0, 5, 9 had much more epithelial cells in LM of lung cancer than primary lung cancer. 152 genes were only expressed in cluster 0, 5, 9 of LM in lung cancer, which might be regarded as the initiating stem genes for LM of lung cancer. And they were enriched in response to dexamethasone and epithelial cell differentiation. 27 clusters have been divided among LM of lung cancer, hepatocellular carcinoma, and primary lung cancer. Cell communication showed that macrophage and cancer associated fibroblasts (CAFs) were the main components for tumor microenvironment, of which migration inhibitor (MIF) (CD74+CXCR4) might be the key signaling pathway for LM of lung cancer.
The initiating stem genes, cellular communication, and regulatory network of tumor microenvironment for LM of lung cancer have been investigated in this study, which provided a further understanding of the potential biological mechanisms of LM in lung cancer.
The authors.
Has not received any funding.
All authors have declared no conflicts of interest.