The Behavior and Role of Lipolysis-stimulated Lipoprotein Receptor, a Component of Tricellular Tight Junctions, in Head and Neck Squamous Cell Carcinomas

Abstract

Background/aim: Lipolysis-stimulated lipoprotein receptor (LSR) knockdown has also been reported to increase the motility and invasiveness of certain cancer cells. Here, we describe, for the first time, the behavior and role of LSR in head and neck squamous cell carcinoma (HNSCC) in vivo and in vitro.

Materials and methods: Samples of HNSCC, normal palatine tonsils, the pharynx carcinoma cell line Detroit562 and primary cultured HNSCC were characterized by immunostaining, western blot, real-time polymerase chain reaction (PCR), Matrigel invasion and proliferation assays.

Results: Protein and mRNA of LSR were strongly expressed, as well as claudin-1 in HNSCC tissues than in normal tissues, especially in invasive tissues. Knock-down of LSR and claudin-1 (CLDN-1), but not tricellulin (TRIC) by siRNAs, markedly induced invasiveness of Detroit562 cells and primary cultured HNSCC. LSR inhibited the development and progression of HNSCC.

Conclusion: LSR is a potential target for new forms of head and neck cancer therapy.

Keywords: Lipolysis-stimulated lipoprotein receptor; claudin; head and neck cancer; tight junctions; tricellulin.