Journal
ANTICANCER RESEARCH
Volume 36, Issue 11, Pages 5895-5904Publisher
INT INST ANTICANCER RESEARCH
DOI: 10.21873/anticanres.11176
Keywords
Lipolysis-stimulated lipoprotein receptor; tricellulin; claudin; tight junctions; head and neck cancer
Categories
Funding
- Ministry of Education, Culture, Sports, Science, and Technology, Japan [25861575]
- Grants-in-Aid for Scientific Research [15K10818, 25861575] Funding Source: KAKEN
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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.
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