Effects of stromal fibroblasts and fat cells and an environmental factor air exposure on invasion of laryngeal carcinoma (HEp-2) cells in a collagen gel invasion assay system.

Effects of stromal fibroblasts and fat cells and an environmental factor air exposure on invasion of laryngeal carcinoma (HEp-2) cells in a collagen gel invasion assay system.
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胶原凝胶侵袭测定系统中基质成纤维细胞和脂肪细胞以及环境因素空气暴露对喉癌 (HEp-2) 细胞侵袭的影响。

DOI:
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发表时间:
1999
期刊:
Archives of Otolaryngology - Head and Neck Surgery
影响因子:
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通讯作者:
Hajime Sugihara
Hajime Sugihara
中科院分区:
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文献类型:
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作者:
S. Yamada;Shuji Toda;Takemoto Shin;Hajime Sugihara

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目的 目的:探讨喉癌细胞(HEp-2)的侵袭机制。 设计 在含有成纤维细胞和/或脂肪细胞的胶原凝胶上培养人HEp-2细胞。HEp-2细胞也用空气暴露作为喉上皮粘膜的局部环境进行处理。在这些培养条件下进行胶原凝胶侵入测定。 结果 在基质无细胞胶原凝胶中没有发现HEp-2细胞的侵袭,但在成纤维细胞包埋的凝胶中观察到轻微的侵袭。HEp-2细胞的更深的侵入发生在成纤维细胞和脂肪细胞共包埋的凝胶和成纤维细胞包埋的凝胶与空气暴露。在成纤维细胞和脂肪细胞共包埋的凝胶结合空气暴露下观察到HEp-2细胞最广泛的侵袭。 结论 脂肪细胞和空气暴露明显增加成纤维细胞在喉鳞状细胞癌中的侵袭作用。这3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着非常重要的作用。这一观察结果表明,肿瘤细胞间质细胞的相互作用和肿瘤细胞局部环境因素的相互作用,应考虑在喉癌的侵袭和增殖机制的调查。
OBJECTIVE To clarify the invasion mechanism of laryngeal carcinoma (HEp-2) cells. DESIGN 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. RESULTS 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. CONCLUSIONS 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.