Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Roles of Podoplanin in Malignant Progression of Tumor

Version 1 : Received: 17 January 2022 / Approved: 19 January 2022 / Online: 19 January 2022 (16:05:50 CET)

A peer-reviewed article of this Preprint also exists.

Suzuki, H.; Kaneko, M.K.; Kato, Y. Roles of Podoplanin in Malignant Progression of Tumor. Cells 2022, 11, 575. Suzuki, H.; Kaneko, M.K.; Kato, Y. Roles of Podoplanin in Malignant Progression of Tumor. Cells 2022, 11, 575.

Journal reference: Cells 2022, 11, 575
DOI: 10.3390/cells11030575

Abstract

Podoplanin (PDPN) is a cell-surface mucin-like glycoprotein that plays a critical role in tumor development and normal development of the lung, kidney, and lymphatic vascular systems. PDPN is overexpressed in several tumors and is involved in their malignancy. PDPN induces platelet aggregation through binding to platelet receptor C-type lectin-like receptor 2. Furthermore, PDPN modulates signal transductions that regulate cell proliferation, differentiation, migration, invasion, epithelial to mesenchymal transition, and stemness, all of which are crucial for the malignant progression of tumor. In the tumor microenvironment (TME), PDPN expression is up-regulated in the tumor stroma, including cancer-associated fibroblasts (CAFs) and immune cells. CAFs play significant roles in the extracellular matrix remodeling and the development of immunosuppressive TME. Additionally, PDPN functions as a co-inhibitory molecule on T cells, indicating the involvement with immune evasion. In this review, we describe the mechanistic basis and diverse roles of PDPN in malignant progression of tumor and discuss the possibility of the clinical application of PDPN-targeted cancer therapy, including cancer-specific monoclonal antibodies, and chimeric antigen receptor T technologies.

Keywords

podoplanin, PDPN, tumor malignancy, tumor marker, antibody therapy, cancer-specific monoclonal antibody, CasMab

Subject

MEDICINE & PHARMACOLOGY, Oncology & Oncogenics

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