In the present study, we discovered that H-TDEs upregulated the expression of FAP, FN, and α-SMA in the fibroblasts and lungs of mice, indicative of the activation of pulmonary fibroblasts, leading to increased secretion of pro-inflammatory cytokines, recruitment of MDSCs, and ultimately increased pulmonary metastatic tumors. The gene discussed is ACTA1; the disease is metastatic neoplasm.