FIBROBLAST-MEDIATED ACCELERATION OF HUMAN EPITHELIAL TUMOR-GROWTH INVIVO
FIBROBLAST-MEDIATED ACCELERATION OF HUMAN EPITHELIAL TUMOR-GROWTH INVIVO
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DOI：
10.1073/pnas.87.1.75
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发表时间：
1990-01-01
影响因子：
11.1
通讯作者：
CHUNG, LWK
中科院分区：
文献类型：
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作者：
CAMPS, JL;CHANG, SM;CHUNG, LWK
与上皮细胞共接种的转化成纤维细胞加速了无胸腺小鼠中人上皮肿瘤的生长并缩短了潜伏期。添加 NbF-1 成纤维细胞导致上皮肿瘤由五种轻微致瘤或“非致瘤”（非肿瘤形成）人类肿瘤细胞系或株生长：PC-3（前列腺）、WH（膀胱）、MDA-436（乳腺癌）以及源自转移性肾盂癌或前列腺癌患者腹水的细胞。通过组织学、免疫组织化学、Southern 杂交和斑点杂交以及细胞遗传学分析提供了这些实验性肿瘤的人类和上皮性质的证据。转化的成纤维细胞主要诱导癌肉瘤，而非致瘤性成纤维细胞（NIH 3T3）和致命照射的转化成纤维细胞仅诱导癌。成纤维细胞-上皮相互作用似乎是双向发生的并且不是由细胞融合引起的。由于体外共培养实验并未证明细胞增殖增加，因此不确定的宿主因素似乎可以影响肿瘤生长。该肿瘤模型可用于药物筛选项目以及调节人类肿瘤生长和进展的因素的机制研究。
Transformed fibroblasts coinoculated with epithelial cells accelerated the growth and shortened the latency period of human epithelial tumors in athymic mice. Addition of NbF-1 fibroblasts caused epithelial tumors to grow from five marginally tumorigenic or "nontumorigenic" (nontumor-forming) human tumor cells lines or strains: PC-3 (prostrate), WH (bladder), MDA-436 (breast), and cells derived from the ascites fluids of patients with metastic renal pelvic or prostate cancers. Evidence for the human and epithelial nature of these experimental tumors was provided by histologic, immunohistochemical, Southern and dot-blot hybridization, and cytogenetic analyses. Transformed fibroblasts induced predominantly carcinosarcomas, whereas nontumorigenic fibroblasts (NIH 3T3) and lethally irradiated transformed fibroblasts induced exclusively carcinomas. The fibroblast-epithelial interaction appears to occur bidirectionally and does not result from cell fusion. Because coculture experiments in vitro did not demonstrate an increased cell proliferation, it appears that undefined host factors can influence tumor growth. This tumor model may be useful in drug-screening programs and in mechanistic studies of factors regulating human tumor growth and progression.