Yamada S, Toda S, Shin T, Sugihara H
Department of Pathology, Saga Medical School, Japan.
Arch Otolaryngol Head Neck Surg. 1999 Apr;125(4):424-31. doi: 10.1001/archotol.125.4.424.
To clarify the invasion mechanism of laryngeal carcinoma (HEp-2) cells.
Human HEp-2 cells were cultured on a collagen gel containing fibroblasts and/or fat cells. The HEp-2 cells were also treated with air exposure as the local environment of the laryngeal epithelial mucosa. A collagen gel invasion assay was conducted under these culture conditions.
No invasion of HEp-2 cells was found in the stromal cell-free collagen gel, but a slight invasion was observed in the fibroblast-embedded gel. A deeper invasion of HEp-2 cells occurred in the fibroblast- and fat cell-coembedded gel and in the fibroblast-embedded gel with air exposure. The most extensive invasion of HEp-2 cells was observed under the fibroblast- and fat cell-coembedded gel in combination with air exposure.
Fat cells and air exposure clearly increase the invasive effect of fibroblasts in squamous cell carcinoma of the larynx. The combined effect of these 3 factors (ie, fat cells, fibroblasts, and air exposure) plays a very important role in the invasive growth of the carcinoma cells. This observation suggests that both tumor cell-stromal cell interaction and tumor cell-local environmental factor interaction should be taken into account in an investigation of the invasive and proliferative mechanisms of laryngeal carcinoma.
阐明喉癌(HEp-2)细胞的侵袭机制。
将人HEp-2细胞培养在含有成纤维细胞和/或脂肪细胞的胶原凝胶上。还将HEp-2细胞暴露于空气中,模拟喉上皮黏膜的局部环境。在这些培养条件下进行胶原凝胶侵袭试验。
在无基质细胞的胶原凝胶中未发现HEp-2细胞侵袭,但在包埋有成纤维细胞的凝胶中观察到轻微侵袭。在包埋有成纤维细胞和脂肪细胞的凝胶以及暴露于空气中的包埋有成纤维细胞的凝胶中,HEp-2细胞出现更深的侵袭。在暴露于空气中的包埋有成纤维细胞和脂肪细胞的凝胶中观察到HEp-2细胞的侵袭最为广泛。
脂肪细胞和空气暴露明显增强了成纤维细胞在喉鳞状细胞癌中的侵袭作用。这三种因素(即脂肪细胞、成纤维细胞和空气暴露)的联合作用在癌细胞的侵袭性生长中起非常重要的作用。这一观察结果表明,在研究喉癌的侵袭和增殖机制时,应同时考虑肿瘤细胞与基质细胞的相互作用以及肿瘤细胞与局部环境因素的相互作用。