Zhou Liang, Xie Ming, Zhou Jia Qing, Tao Lei
Department of Otolaryngology, Eye and ENT Hospital, FuDan University, Shanghai, China.
Laryngoscope. 2006 Jan;116(1):28-32. doi: 10.1097/01.mlg.0000184505.05662.b9.
OBJECTIVES/HYPOTHESIS: Abnormal interaction of epithelial cells with laminin component of basement membrane may account for altered biological behavior of cells, influencing proliferation, adhesion, and motility. In the current study, we investigated the role of 67-kDa laminin receptor (67LR), a high affinity receptor for laminin, in aggressiveness of laryngeal squamous cell carcinoma.
Thirty paraffin-embedded specimens and 20 fresh tissues of patients with laryngeal squamous cell carcinoma were analyzed using immunohistologic and reverse-transcriptase polymerase chain reaction techniques, respectively. Expression of 67LR on the surface of AMC-HN-8 cells was examined by flow cytometry. The effect of 67LR monoclonal antibody (MLuC5) on the adhesive and invasive abilities of AMC-HN-8 cells was determined by adherence and invasion inhibition assay in vitro.
Both at the mRNA and protein level, laryngeal carcinoma cells expressed higher level of 67LR than normal epithelial cells (P < .01). The expression of 67LR correlated inversely with differentiation extent of tumor (P < .05). 67LR level was significantly increased in patients with lymph node metastases than those without lymph node involvement (P < .05). Flow cytometry showed 80.9 +/- 0.9% of AMC-HN-8 cells expressed 67LR. After 60 minutes and 120 minutes of incubation, MluC5 induced 57.1 +/- 3.6% and 63.2 +/- 2.8% inhibition of adhesion, respectively. The invasive ability of AMC-HN-8 cells to matrigel was reduced by MLuC5.
Laryngeal carcinoma cells over-expressing 67LR have a stronger aggressive potential, which might make 67LR a promising target for the treatment of metastatic tumor.
目的/假设:上皮细胞与基底膜层粘连蛋白成分的异常相互作用可能导致细胞生物学行为改变,影响细胞增殖、黏附和迁移。在本研究中,我们调查了层粘连蛋白高亲和力受体67-kDa层粘连蛋白受体(67LR)在喉鳞状细胞癌侵袭性中的作用。
分别采用免疫组织学和逆转录聚合酶链反应技术分析30例喉鳞状细胞癌患者的石蜡包埋标本和20例新鲜组织。通过流式细胞术检测AMC-HN-8细胞表面67LR的表达。采用体外黏附及侵袭抑制试验,检测67LR单克隆抗体(MLuC5)对AMC-HN-8细胞黏附和侵袭能力的影响。
在mRNA和蛋白水平上,喉癌细胞中67LR的表达水平均高于正常上皮细胞(P <.01)。67LR的表达与肿瘤分化程度呈负相关(P <.05)。有淋巴结转移的患者67LR水平显著高于无淋巴结转移者(P <.05)。流式细胞术显示80.9±0.9%的AMC-HN-8细胞表达67LR。孵育60分钟和120分钟后,MLuC5分别诱导57.1±3.6%和63.2±2.8%的黏附抑制。MLuC5降低了AMC-HN-8细胞对基质胶的侵袭能力。
过表达67LR的喉癌细胞具有更强的侵袭潜能,这可能使67LR成为转移性肿瘤治疗的一个有前景的靶点。