脂肪分解刺激脂蛋白受体（一种三细胞紧密连接成分）在头颈部鳞状细胞癌中的行为及作用
The Behavior and Role of Lipolysis-stimulated Lipoprotein Receptor, a Component of Tricellular Tight Junctions, in Head and Neck Squamous Cell Carcinomas.
作者信息
Takano Kenichi, Kakuki Takuya, Obata Kazufumi, Nomura Kazuaki, Miyata Ryo, Kondo Atsushi, Kurose Makoto, Kakiuchi Akito, Kaneko Yakuto, Kohno Takayuki, Himi Tetsuo, Kojima Takashi
机构信息
Department of Otolaryngology, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan
Department of Otolaryngology, Research Institute for Frontier Medicine, Sapporo Medical University School of Medicine, Sapporo, Japan.
出版信息
Anticancer Res. 2016 Nov;36(11):5895-5904. doi: 10.21873/anticanres.11176.
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.
背景/目的：据报道，脂解刺激脂蛋白受体（LSR）的敲低也会增加某些癌细胞的运动性和侵袭性。在此，我们首次描述了LSR在头颈部鳞状细胞癌（HNSCC）体内和体外的行为及作用。
材料与方法
通过免疫染色、蛋白质印迹、实时聚合酶链反应（PCR）、基质胶侵袭和增殖试验，对HNSCC样本、正常腭扁桃体、咽癌细胞系底特律562和原代培养的HNSCC进行特征分析。
结果
与正常组织相比，尤其是在侵袭性组织中，HNSCC组织中LSR的蛋白质和mRNA以及闭合蛋白-1均高表达。小干扰RNA（siRNAs）敲低LSR和闭合蛋白-1（CLDN-1），而非三细胞连接分子（TRIC），可显著诱导底特律562细胞和原代培养的HNSCC的侵袭性。LSR抑制HNSCC的发生和进展。
结论
LSR是头颈部癌症新型治疗的潜在靶点。
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