FIGURE 3.

Screening, selection and validation of target gene long‐chain acyl‐coenzyme A synthases 5 (ACSL5) in lysophosphatidylcholine (lysoPC) effects. (A) The lysoPC‐specific genes and pathways using RNA‐seq were screened and selected in cells treated with vehicle or lysoPC for 24 h, by matching human lipid‐related genes for pathway enrichment (https://metascape.org/). Of the top 50 differently expressed genes related to fatty acid metabolism (B), ACSL family members, for example, ACSL1, ACSL3, ACSL4 and ACSL5 over‐expressed 6 and 24 h after treatment with lysoPC and presented digitally in (C) (n = 3 per time point and n = 6 per group). Of the ACSL family, the overall survival rate (OS) and progression‐free survival rate (PFS) of lung cancer or adenocarcinoma (ADC) patients with ACSL5 high‐ and low‐expression were validated using Kaplan‐Meier Plotter of survival data (D). Spatial expression of ACSL5 in preclinical lung cancer tissues was measured by intra‐tumoural immunohistochemistry detection of the ACSL5 gene in mice model (E). The expression (F; n = 27) and heatmap (G) of ACS family member genes were validated in lung single epithelial cells from lung tissues of normal (n = 20), chronic obstructive pulmonary diseases (COPD; n = 15), idiopathic pulmonary fibrosis (IPF; n = 15), lung adenocarcinoma (ADC; n = 15), systemic sclerosis‐associated interstitial lung disease (SSC; n = 8) or para‐cancerous tissue (para‐cancer; n = 11) by deep‐mining of single‐cell RNA‐seq datasets (GSE128169, GSE131907 and GSE136831). * and ** stand for the p‐values less than .05 and .01, respectively, as compared with the groups treated with vehicle or healthy