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

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

  • J Invest Dermatol. 2022 Feb;142(2):303-313.e9. doi: 10.1016/j.jid.2021.07.163.
Yingjian Huang 1 Yuqian Wang 1 Yan Wang 2 Ning Wang 1 Qiqi Duan 1 Shengbang Wang 1 Meng Liu 1 Muhammad Ahsan Bilal 1 Yan Zheng 3
Affiliations

Affiliations

  • 1 Department of Dermatology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
  • 2 Center for Mitochondrial Biology and Medicine, The Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an, China.
  • 3 Department of Dermatology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China. Electronic address: zenyan66@126.com.
Abstract

Cutaneous squamous cell carcinoma (cSCC) is the second most common form of skin Cancer. LPCAT1, a lysophosphatidylcholine Acyltransferase, takes a center stage in 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 this study, we found that LPCAT1 was upregulated in cSCC tissues and in 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, and enhanced cell metastasis. Mechanistically, LPCAT1 regulated EGFR signaling. The oncogenic effect of LPCAT1 was mediated by EGFR/protein kinase B and EGFR/p38MAPK pathways in cSCC. Using the xenograft mouse model, we consolidated the results mentioned earlier. In conclusion, LPCAT1 contributed to cSCC progression through EGFR-mediated protein kinase B and p38MAPK signaling pathways. LPCAT1 may serve as a target for therapeutic intervention in cSCC.

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