LPCAT1 Promotes Cutaneous Squamous Cell Carcinoma via EGFR-Mediated Protein Kinase B/p38MAPK Signaling Pathways

Cutaneous squamous cell carcinoma (cSCC) is the second most common form of skin cancer. LPCAT1, a lysophosphatidylcholine acyltransferase, takes a center stage in the membrane lipid remodeling. LPCAT1 is elevated in several cancers and contributes to cancer development. However, its role and molecular mechanisms in cSCC remain to be elucidated. In the present study, we found that LPCAT1 was up-regulated in cSCC tissues and cell lines. In vitro, loss-of-function and gain-of-function experiments demonstrated that LPCAT1 facilitated cSCC cell proliferation, protected cells against apoptosis, accelerated epithelial-mesenchymal transition (EMT), and enhanced cell metastasis. Mechanistically, LPCAT1 regulated EGFR signaling. The oncogenic effect of LPCAT1 was mediated by EGFR/AKT and EGFR/p38MAPK pathways in cSCC. Using the xenograft mouse model, we consolidated the above results. In conclusion, LPCAT1 contributed to cSCC progression via EGFR-mediated AKT and p38MAPK signaling pathways. LPCAT1 may serve as a novel target for therapeutic intervention.